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Table of Contents

Reviewed August 8, 2003

Richard A.
Grimm, DO

Department of
Cardiovascular
Medicine

Barbara
Hesse, MD

Department of
Cardiovascular
Medicine

Copyright 2003
The Cleveland Clinic Foundation

ACUTE PERICARDITIS

ACUTE
PERICARDITIS

     Definition

     Prevalence

     Etiology

     Signs and
     Symptoms

     Diagnosis

     Therapy

     Outcomes

     Definition

     Etiology

     Pathophysiology

     Diagnosis

     Therapy

     Outcomes

     Definition

     Prevalence

     Pathophysiology

     Signs and
     Symptoms

     Diagnosis

     Therapy

     Definition

     Etiology

     Pathophysiology

     Signs and
     Symptoms

     Diagnosis

     Therapy

     Outcomes

Acute pericarditis is an inflammatory process involving the pericardium, resulting in a clinical syndrome with the triad of chest pain, pericardial friction rub, and electrocardiographic (ECG) changes.¹

Acute pericarditis is the admitting diagnosis in 0.1% of hospital admissions. It occurs more commonly in men than in women.

The most common form of acute pericarditis is idiopathic (Table 1). Other common causes include infection, renal failure, myocardial infarction (MI),² malignancy, radiation, and trauma.³ These different etiologies are discussed in more detail below.

Symptoms:
The most common symptom of acute pericarditis is severe, sharp, retrosternal chest pain, often radiating to the neck, shoulders, or back. Positional changes are characteristic, with worsening of the pain in the supine position and with inspiration, and improvement with sitting upright and leaning forward. Other symptoms may occur, reflecting the underlying disease.

Physical Examination:

A scratchy, grating, high-pitched friction rub ("squeak of leather of a new saddle") that is due to fibrinous deposits in the pericardial space (Figure 1) with three components—atrial systole, ventricular systole, and early ventricular diastole—is classic. It is best heard during inspiration at the left lower sternal border, with the patient leaning forward. The rub may disappear with the development of an effusion and impending cardiac tamponade.¹

Specific Types of Acute Pericarditis:

Idiopathic Pericarditis
The etiology of acute pericarditis is often difficult to establish, and idiopathic pericarditis remains the most common diagnosis.

Viral Pericarditis
Coxsackievirus B and echovirus are the most common viruses, and a fourfold increase in antiviral titers is required for the diagnosis. Patients often experience a prodrome of an upper respiratory tract infection. The prognosis of viral pericarditis is good, the course is usually self-limited, and patients may be treated on an outpatient basis.

Purulent Pericarditis
Before the antibiotic era, pneumonia was the prime cause of purulent pericarditis. Contemporary causes include thoracic surgery, chemotherapy, immunosuppression, and hemodialysis. Presentation is usually acute with high fevers, chills, night sweats, and dyspnea, but the classic findings of chest pain or friction rub are rare. Cardiac tamponade occurs frequently (42%-77% of patients in selected series), and mortality is high. If purulent pericarditis is suspected, hospital admission with immediate pericardiocentesis and intravenous broad-spectrum antibiotics is mandatory, followed by early surgical drainage. Findings on pericardial fluid analysis include a high protein (>6 g/dL), low glucose (<35 mg/dL), and very high leukocyte count (6,000-240,000/mm³).⁴

Tuberculous pericarditis⁵ occurs in 1% to 2% of cases of pulmonary tuberculosis. Immunocompromised or human immunodeficiency virus-positive patients are at increased risk. Nonspecific symptoms such as dyspnea, fever, chills, and night sweats develop slowly, and a friction rub or chest pain is often absent. The ECG is usually unrevealing, but the chest radiograph may be most useful when findings of pulmonary tuberculosis are present (Figures 2,3). A patient with suspected or diagnosed pericardial tuberculosis should be hospitalized, and antituberculous therapy (rifampin, isoniazid, streptomycin, and ethambutol) started promptly.

Analysis of the pericardial fluid shows high specific gravity, very high protein (often >6 g/dL), and predominantly lymphocytic cells. A pericardial biopsy with acid-fast bacilli polymerase chain reaction testing is recommended in all patients with suspected tuberculous pericarditis. However, a normal pericardial biopsy does not exclude the diagnosis.

Uremic and Dialysis-associated Pericarditis
Uremic pericarditis occurs in 6% to 10% of patients with advanced renal failure before the initiation of hemodialysis; blood urea nitrogen levels usually exceed 60 mg/dL. The typical ST-segment elevation on the ECG usually is absent. A large, hemorrhagic effusion because of impaired platelet function is common, although tamponade is rare. Dialysis-associated pericarditis is caused by fluid overload, and the fluid is usually serous. With both forms, institution or intensification of hemodialysis is indicated, usually leading to improvement in 1 to 2 weeks.^6,7

Postmyocardial infarction pericarditis is a common complication (25%-40% of patients with MI) and occurs early, within 3 to 10 days after the MI. The incidence correlates with the extent of necrosis and occurs more frequently with anterior than with inferior infarcts, and is associated with a higher 1-year mortality and incidence of congestive heart failure.⁸

The diagnosis of post-MI pericarditis requires symptoms or a new pericardial friction rub; a pericardial effusion alone is nonspecific. Beside the typical ST elevation seen with acute pericarditis that may be difficult to differentiate from the actual MI in this setting, ECG findings are persistently positive T waves more than 2 days post-MI or normalization of previously inverted T waves.⁹

Postcardiac Injury Syndrome
"Dressler's syndrome" typically occurs 2 to 3 weeks after MI or open-heart surgery. An autoimmune component and possibly a latent viral infection are thought to be responsible. The fully expressed syndrome consists of pleuritic chest pain, fever, leukocytosis, and a pericardial friction rub. Pleural effusions or pulmonary infiltrates may be seen.¹⁰

Malignancy
Pericarditis associated with malignancy is due mostly to metastatic disease. Bronchogenic or breast carcinoma, Hodgkin's disease, and lymphoma are common (Figure 4); primary mesothelioma and angiosarcoma are rare. Diagnosis is based on analysis of pericardial fluid cytology, which has a sensitivity ranging from 70% to 90% and a specificity up to 95% to 100%.¹

Radiation Pericarditis
Recent or remote mediastinal radiation may cause pericarditis anywhere from weeks to months after the exposure.

Traumatic Pericarditis
Sharp or blunt trauma (Figure 5) and even minimally invasive procedures such as cardiac diagnostic or interventional catheterizations have been associated with pericardial irritation.

The diagnosis of acute pericarditis remains a clinical diagnosis based on history, physical examination, and the ECG. Other imaging studies, including computed tomography (CT), magnetic resonance imaging (MRI), and echocardiography, may be used in selected cases to investigate the pericardium.

Electrocardiogram
The ECG in acute pericarditis has four consecutive stages (Table 2). Stage 1, characterized by diffuse ST elevation, is the most useful stage for the diagnosis of acute pericarditis (Figure 6). The distinction between pericarditis and acute MI is difficult at times, but there are several clues (Table 3).¹¹

Chest Radiograph
The chest radiograph may be entirely normal unless there is a pericardial effusion causing cardiomegaly (Figure 7) or changes due to an underlying disease.

Echocardiography
An episode of acute pericarditis that responds well to therapy may be followed clinically. Indications for echocardiography are symptoms persisting for longer than 1 to 2 weeks; the presence of hemodynamic abnormalities; clinical suspicion of a large or increasing pericardial effusion; or recent cardiac surgery.

Most cases of acute pericarditis are uncomplicated and self-limited, and may be treated on an outpatient basis. Indications for an imaging modality and/or hospital admission include clinical suspicion of a large effusion, hemodynamic instability, severe pain or other symptoms, suspicion of a serious underlying condition, or any other signs or symptoms of clinical instability or impending deterioration.

Medical Management
Treatment of the underlying disease is the mainstay of therapy.¹²

Nonsteroidal anti-inflammatory drugs (NSAIDS) such as oral indomethacin are effective for relief of pain. Of note, NSAIDS are contraindicated in the early period (<7-10 days) after MI (causing increased coronary vasospasm), and aspirin should be used instead.

If pericarditis recurs (20%-30% of patients) or response to NSAIDS is poor, prednisone may be started at high doses and then tapered over 3 weeks. As with NSAIDS, steroids should be avoided in post-MI pericarditis since there is increased incidence of myocardial wall rupture.

Colchicine may be effective in persistent or refractory cases of Dressler's syndrome and idiopathic pericarditis.^13,14

If not mandatory, anticoagulants should be held off during the acute phase of pericarditis to reduce the risk of bleeding and tamponade.

Pericardiectomy
Indications for pericardiectomy are recurrent pericarditis or the development of pericardial constriction. Pericardiectomy is the most definitive procedure with virtually no recurrence; 30-day perioperative mortality is about 5%.

Pericardial effusion is defined as an increased amount of pericardial fluid.

Common causes are listed in Table 1. The most common causes of large pericardial effusions are malignancy (25% of cases), infection (27%), collagen vascular disease (12%), and chest radiation (14%).^15,16 A pericardial effusion is the most common cardiovascular presentation of acquired immune deficiency syndrome and is associated with worse outcome.^17-19

The pericardial sac normally contains 15 to 30 mL of fluid (Figure 8); it can hold 80 to 200 mL of fluid acutely and even up to 2 liters if the fluid accumulates slowly (Figure 9). The development of tamponade depends on the rate of accumulation rather than the effusion size. Typically, signs of right ventricular diastolic failure develop first, followed by left-sided symptoms.

Physical Examination
With a small effusion, the physical examination is unremarkable. Larger effusions cause muffled heart sounds and, rarely, Ewart's sign (dullness to percussion, bronchial breath sounds, and egophony below the angle of the left scapula). With increasing size of the effusion, signs and symptoms of cardiac tamponade may occur (see section III, Cardiac Tamponade).

Electrocardiography
Low voltage and electrical alternans (Figure 10) may be seen if the effusion is large.

Chest Radiography
Cardiomegaly occurs if there is more than 250 mL of fluid in the pericardial sac (Figure 7). Displacement of the pericardial lining >2 mm away from the lower heart border is best seen on lateral film.^20,21

Echocardiography
A pericardial effusion causes an echo-free space between visceral and parietal pericardium; the extent of the space defines the size of the effusion (Table 4). Large effusions may produce the picture of a "swinging heart" (Figure 10). Although echocardiography is the imaging modality of choice for diagnosing a pericardial effusion, it may miss small, loculated effusions.

Magnetic Resonance Imaging and
Computed Tomography
MRI is the best imaging modality for assessing the pericardium itself, being slightly superior to CT in spatial resolution. Both are superior to echocardiography in detecting loculated effusions.

Laboratory Tests
Laboratory analysis in a patient with a pericardial effusion should include a serum complete blood count, chemistry panel, and erythrocyte sedimentation rate. Further testing should be done according to clinical suspicion.

Analysis of Pericardial Fluid
Pericardiocentesis should be performed for diagnostic purposes if the etiology is unclear or if malignancy or tuberculous, fungal, or bacterial infection is suspected. Therapeutic pericardiocentesis should be performed for large effusions that are increasing in size or those causing pretamponade or tamponade.

The initial inspection should assess whether the fluid is hemorrhagic, purulent, or chylous. A red blood cell count >100,000/mm³ is suggestive of trauma, malignancy, or pulmonary embolism (rare). Chylous fluid implies injury to the thoracic duct by trauma or infiltration. The fluid should be sent for a cell count, Gram's stain and culture, cytology, acid-fast bacilli, glucose, protein, lactate dehydrogenase (LDH), and specific gravity. The parameters listed in Table 5 have a high sensitivity for differentiating exudates versus transudates. An elevated protein level >6.0 g/dL often indicates tuberculous, purulent, or parapneumonic effusion. Isolated increased fluid LDH (>300 U/dL) with normal serum LDH is most likely due to malignancy. Low pericardial fluid glucose level (<60 to 80 mg/dL) may be due to parapneumonic, rheumatoid, tuberculous, or malignant effusion. However, no diagnostic test of pericardial fluid is specific for effusion associated with postpericardiotomy syndrome, radiation or uremic pericarditis, hypothyroidism, or trauma. The overall diagnostic yield of pericardial fluid analysis and biopsy is low (about 20%), emphasizing the importance of clinical history and examination.⁴

The medical management of pericardial effusion is based on treating the underlying cause.²² Diuretics may help to decrease the intensity of fluid overload symptoms if such are present. Effusions causing pretamponade or tamponade require immediate drainage. Volume expansion and inotropic support may be used for hemodynamic stabilization pending drainage. In the immediate postoperative setting, surgical management and open drainage are preferred because of the high incidence of loculated effusions.

Pericardiocentesis
Echocardiography-guided pericardiocentesis is safe and effective. Indications for pericardiocentesis include large effusion with hemodynamic compromise, tamponade, or diagnostic purposes.

Surgical Management:

Percutaneous Balloon Pericardiotomy
This is the least invasive of the surgical procedures, and is used mostly for neoplastic effusion with a poor prognosis as a palliative treatment option. The success rate for relieving reaccumulation of pericardial fluid is 85% to 92% at 30 days. It may be performed in the catheterization laboratory under fluoroscopy using a balloon dilating catheter.

Subxyphoid Pericardiostomy
This procedure, known as "pericardial window," may be done under local anesthesia. It has a high success rate with few complications, and recurrence of fluid accumulation is rare.

After drainage, follow-up echocardiography to rule out reaccumulation and constrictive physiology should be performed in all patients. Cardiac tamponade may develop with large or rapidly accumulating effusions.

Twenty-five percent to 30% of patients with large pericardial effusions develop tamponade.²⁴

Physical Examination
The combination of the classic findings known as Beck's triad (hypotension, jugular venous distention, and muffled heart sounds) occurs in only 10% to 40% of patients. Tachycardia, tachypnea, and hepatomegaly are common. Pulsus paradoxus is defined as inspiratory decline in systolic blood pressure >10 mm Hg, caused by compression and poor filling of the left ventricle due to increased venous return to the right side of the heart. Pulsus paradoxus is nonspecific and insensitive, and it may occur with extracardiac diseases such as severe chronic obstructive pulmonary disease or asthma.²⁷

Transthoracic Echocardiography
Usually, a moderate-size or large pericardial effusion is present (Figure 9) and leads to increasing compression and subsequent diastolic collapse of the cardiac chambers, usually in the sequence right atrium—right ventricle—left atrium. The most sensitive finding for tamponade physiology on the echocardiogram is inferior vena cava plethora with absent inspiratory collapse. Right ventricle collapse is the most accurate finding for diagnosis. Other nonspecific findings include excessive respiratory variations in diastolic atrioventricular valve flow.

Right Heart Catheterization
The most typical finding of right heart catheterization is equalization of mean right atrial, right ventricular and pulmonary artery diastolic, and mean pulmonary capillary wedge pressures.

Differential Diagnosis
The symptoms of pericardial tamponade may mimic right-sided heart failure, right ventricle infarction, constrictive pericarditis, and pulmonary embolism. However, with the use of echocardiography and right heart catheterization, these may be easily distinguished.

Constrictive pericarditis refers to an abnormal thickening of the pericardium, resulting in impaired ventricular filling and decreased cardiac output.

Clinical Symptoms
Symptoms are often vague and their onset is insidious, and include malaise, fatigue, and decreased exercise tolerance. With progression of constriction, symptoms of right-sided heart failure (peripheral edema, nausea, abdominal discomfort, ascites) become apparent and usually precede signs of left-sided failure (exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea).

Physical Examination
Increased ventricular filling pressures cause jugular venous distention and Kussmaul's sign, (absent inspiratory decline of jugular venous distention), which is sensitive but nonspecific for constriction.²⁹ Auscultation reveals muffled heart sounds and occasionally a characteristic pericardial knock (60-200 msec after the second heart sound), caused by sudden termination of ventricular inflow by the encasing pericardium.

Constrictive-Effusive Pericarditis
This entity consists of a tense pericardial effusion in the presence of pericardial constriction, and both tamponade and constrictive signs and symptoms are present. Therapy includes pericardiocentesis initially, followed by pericardiectomy for long-term management.³⁰

Electrocardiograph
ECG does not show specific findings, but low voltage may be seen.

Chest Radiograph
Pericardial calcifications (Figures 2 and 3), pleural effusions, and bi-atrial enlargement may be noted on chest radiograph.

Echocardiography
This is the best imaging modality for assessing hemodynamic parameters noninvasively. M-mode echocardiography is useful to look for flattening of the left ventricular free wall. Two-dimensional echocardiography shows septal bounce and inferior vena cava plethora with absent inspiratory collapse. Doppler-echocardiographic findings have the highest sensitivity and specificity for detecting constrictive physiology. Excessive respiratory variations in transmitral, transtricuspid, pulmonary venous, and hepatic vein flow are characteristic.^31,32

Right Heart Catheterization
Direct pressure measurements are performed if there is doubt about the diagnosis. M- or W-shaped atrial pressure waveforms and "square root" or "dip-and-plateau" right ventricular pressure waveforms reflect impaired ventricular filling. Because of the fixed and limited space within the thickened and stiff pericardium, end-diastolic pressure equalization (typically within 5 mm Hg) occurs between these cardiac chambers.

Magnetic Resonance Imaging
and Computed Tomography
MRI is the imaging modality of choice to evaluate the pericardium, being slightly superior to CT in spatial resolution. Pericardial calcifications may easily be identified on CT (Figure 13).

Recurrence following surgery is caused mainly by incomplete resection. Without surgical treatment, biventricular heart failure develops.

Return to Medicine Index

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