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Mangi AA, Torchiana DF. Pericardial Disease.
In: Cohn LH, Edmunds LH Jr, eds. Cardiac Surgery in the Adult. New York: McGraw-Hill, 2003:13591372.

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Chapter 57

Pericardial Disease

Abeel A. Mangi/ David F. Torchiana

ANATOMY AND FUNCTION
PATHOPHYSIOLOGY OF PERICARDIAL COMPRESSION
????Tamponade
????Constriction
CONGENITAL ABNORMALITIES
ACQUIRED ABNORMALITIES
????Infectious Pericarditis
????????VIRAL PERICARDITIS
????????BACTERIAL (SUPPURATIVE) PERICARDITIS
????????TUBERCULOUS PERICARDITIS
????????FUNGAL PERICARDITIS
????Metabolic Causes of Pericarditis
????????UREMIC PERICARDITIS
????????DRUG-INDUCED PERICARDITIS
????????PERICARDITIS ASSOCIATED WITH RHEUMATOID ARTHRITIS
????????HYPOTHYROIDISM
????Radiation Pericarditis
????Neoplastic Pericarditis
????Traumatic Pericardial Disease
????????PENETRATING TRAUMA
????????BLUNT TRAUMA
????Peridcarditis Associated with Myocardial Infarction/Dressler Syndrome
????Cardiac Surgery and the Pericardium
????????POSTINFARCTION PERICARDITIS
????????POSTPERICARDIOTOMY SYNDROME
????????LATE CARDIAC TAMPONADE
????????PERICARDIAL CLOSURE
OPERATIONS
????Mediastinal Reexploration
????Pericardiocentesis
????Pericardial Window
????Pericardial Stripping
ACKNOWLEDGMENTS
REFERENCES

?? INTRODUCTION
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The pericardium invests the heart like a cocoon; when incised and suspended from a chest retractor it nicely presents the heart for surgical correction. The surgical significance of the pericardium arises when cardiac filling is perturbed. When the limited space between the rigid pericardium and heart is acutely filled with blood or fluid, cardiac compression and tamponade may result. When inflammation and scarring cause the pericardium to shrink and densely adhere to the surface of the heart, constrictive pericarditis is the consequence. In this chapter, we will discuss pericardial anatomy and function and describe the conditions that commonly give rise to pericardial constriction and tamponade. The chapter includes steps for the diagnosis and therapy of these entities, the management of tamponade that occurs late after cardiac surgery, and the rationale for and against pericardial closure at the time of cardiac surgery.


?? ANATOMY AND FUNCTION
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The pericardium serves two major functions: (1) to maintain the position of the heart within the mediastinum, and (2) to prevent cardiac distension by sudden volume overload. The position of the pericardium is maintained by loose attachments to the undersurface of the sternum and to the vertebral bodies, and by firm attachment to the central tendon of the diaphragm. The pericardium attaches to the ascending aorta, just inferior to the innominate vein, and attaches to the superior vena cava (SVC) several centimeters above the sinoatrial node. The pericardial reflection encompasses the superior and inferior pulmonary veins, and encircles the inferior vena cava (IVC), thereby making it possible for the surgeon to control the IVC from within the pericardium. The pericardial reflection attaches to the left atrium near the entrances of the pulmonary veins just above the atrioventricular groove (Fig. 57-1). The pericardium is perfused by the pericardiophrenic arteries that travel with the phrenic nerves, as well as by branches of the internal mammary arteries and feeder branches directly from the aorta. It is innervated by vagal fibers from the esophageal plexus, and the phrenic nerves course within it.



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FIGURE 57-1 Pericardial attachments and reflections. PA = pulmonary artery; PV = pulmonary vein; IVC = inferior vena cava; SVC = superior vena cava.

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The pericardium is made up of two layers. The inner layer (visceral layer) of the pericardium is transparent, and is made up of a monolayer of mesothelial cells, making it essentially indistinguishable from the epicardium. Parietal pericardial lymphatic drainage is largely to the anterior and posterior mediastinal nodes, whereas visceral pericardial lymphatic drainage is via the tracheal and bronchial mediastinal lymph nodes.1 The pericardial mesothelial cells contain dense microvilli that are 1?m wide and 3?m high,2 ideal for facilitating fluid and ion exchange.3

The parietal layer is made up of elastin fibers interspersed amongst dense parallel bundles of collagen, which render this layer relatively noncompliant. Because the pericardium is stiffer than cardiac muscle, it tends to equalize the compliance of both chambers. By doing so, the pericardium contributes to the resting cavitary diastolic pressure of both ventricles, maximizing diastolic ventricular interaction.4 An example of this phenomenon is the diminution of systemic arterial pressure during inspiration. Intrapericardial pressure tends to approximate pleural pressure, and varies with respiration. The negative intrathoracic pressure generated during inspiration augments right ventricular filling. The interventricular septum shifts towards the left to accommodate the increase in right ventricular volume. Because pericardial constraint does not allow equal filling of the left ventricle, the decrease in volume ejected by the systemic chamber results in a slight diminution of systemic arterial pressure during inspiration. This phenomenon is greatly magnified with an increase in intrapericardial pressure (for example, during acute filling of the pericardial space, or circulatory volume overload) resulting in production of the pulsus paradoxus.57

Normally, the volume of the pericardium exceeds that of the heart by about 10% to 20%.8 The pericardium contains several sinuses and recesses that are not readily evident at the time of surgery or at postmortem examination (see Fig. 57-1). The largest (the transverse pericardial sinus) is the space between the ascending aorta and pulmonary artery bifurcation anteriorly, and the dome of the left atrium and SVC posteriorly. Such potential spaces allow the pericardium to expand and accommodate a limited volume load. Under normal conditions, the pericardium contains approximately 20 mL of fluid, which is an ultra-filtrate of plasma. This pericardial fluid serves to lubricate the junction of the beating heart with fixed structures.9 The relative noncompliance of the pericardium results in a nonlinear relationship between intrapericardial volume and intrapericardial pressure. Although the pericardium may gradually expand to accommodate large volumes over time without appreciable increases in intrapericardial pressure, an acute volume overload may result in a large increase in intrapericardial pressure (Fig. 57-2). The pathophysiological sequelae of pericardial compliance and pericardial constraint are discussed below.



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FIGURE 57-2 Relationship of intrapericardial volume and pressure. The pericardium of a healthy individual can accommodate 15 to 20 mL of fluid, with minimal increases in intrapericardial pressure. However, when the elastic limit of the pericardial space is acutely exceeded, small increases in intrapericardial volume will result in large increases in intrapericardial pressure (solid line). Intrapericardial volume and pressure are not linearly related. With gradual development of an effusion, the pericardial space can dilate considerably (dashed line). It may therefore accommodate a relatively large effusion without an appreciable increase in intrapericardial pressure. (Modified with permission from Harken AH, Hammond GL, Edmunds LH Jr: Pericardial diseases, in Edmunds LH Jr (ed): Cardiac Surgery in the Adult. McGraw-Hill, New York, 1996; p 1303.)

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?? PATHOPHYSIOLOGY OF PERICARDIAL COMPRESSION
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Tamponade

Tamponade is a state of circulatory decompensation that results from cardiac compression due to increased intrapericardial pressure. The clinical syndrome of tamponade varies widely, and is a reflection of the severity of hemodynamic impairment as well as the physiologic resilience of the host. Although hemorrhage is the most common etiology, pericardial diseases of almost any type can produce tamponade. It can be due to the accumulation of effusions, blood, clots, pus, or gas, or any combination of these. When pericardial filling commences, pericardial reserve volume (1020 mL) is rapidly depleted. As fluid enters the pericardial space faster than the rate at which the parietal pericardium stretches, the noncompliant parietal pericardium prevents further expansion. At this point, pericardial volume can only increase by reducing cardiac chamber volumes. As a result, diastolic compliance is reduced equally in all chambers of the heart. This loss in compliance, coupled with the increase in intrapericardial pressures, means that higher pressures are required to fill the cardiac chambers, which may be partially achieved by parallel increases in systemic and pulmonary venous pressure by vasoconstriction.10,11 Other compensatory mechanisms include tachycardia, time-dependent pericardial stretch, and blood volume expansion.12 The latter two mechanisms are of little help in acute tamponade. The rapid accumulation of as little as 150 mL of fluid in the pericardial space (for example, after a penetrating cardiac wound) does not allow the parietal pericardium to develop any degree of compliance. In such a setting, the rapid accumulation of a relatively small volume of blood in the pericardial space can result in critical tamponade. On the other hand, the gradual accumulations of large pericardial effusions (over 1 L) can be compensated for in a more chronic setting such as inflammatory conditions. Distension of the pericardial space can be detected by chest roentgenogram (Fig. 57-3) or echocardiogram (Fig. 57-4).



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FIGURE 57-3 Enlarging pericardial effusion detected on chest x-ray. (A) At discharge; (B) on re-presentation, 3 weeks after discharge.

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FIGURE 57-4 Large pericardial effusion detected on echocardiogram. LA = left atrium; LV = left ventricle; RV = right ventricle; PE = pericardial effusion.

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Constriction

A wide range of disease processes can result in formation of a pericardial scar, the basic pathologic process behind constrictive pericarditis. The principal etiologies behind pericardial scar formation have changed over the last 25 years. The incidence of infectious etiologies (particularly tuberculosis) has declined, whereas the incidence of cases resulting from therapeutic irradiation of the mediastinum, cardiac surgery, and trauma (Fig. 57-5) has been increasing.13 Constrictive pericarditis is important to recognize, because it is curable.



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FIGURE 57-5 Pericardial calcification on PA (A) and lateral (B) chest x-ray in a young patient with a history of thoracic trauma.

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Pericardial constriction exerts its pathophysiological effects by limiting cardiac filling. Unlike cardiac tamponade, in which cardiac filling is limited from the very beginning of diastole, constriction does not restrict filling in the earliest stages of diastole. As the ventricles fill, they are prevented from their normal distention as they encounter a stiff, contracted, and noncompliant pericardium. As a result, 70% to 80% of diastolic filling is forced to occur in the first 25% to 30% of diastole.14 Although early diastolic filling pressures are normal (while the ventricle is free from the overlying stiff pericardium), later diastolic filling pressures are much higher. This sudden increase in diastolic pressure is reflected in the "dip and plateau" or "square-root" sign (Fig. 57-6), which occurs when ventricular pressures are measured during cardiac catheterization. On this tracing, the gradual onset of diastolic filling is interrupted by an abrupt dip as the ventricles encounter the constrictive pericardium. The relaxing ventricles then spring back and reach the limit of the constrictive pericardium, generating a gentle rise in diastolic pressure that manifests itself as a plateau tracing. Similarly, right atrial pressure tracings reveal a deep y descent, which correlates to the nadir of the "square-root" sign. The clinical manifestation of this phenomenon is seen in the Kussmaul sign. Under normal circumstances, inspiration results in a 3- to 7-mm Hg drop in right atrial pressure. Venous flow from the neck veins therefore accelerates into the heart. The high pressure of pericardial constriction prevents the right atrium from accepting inspiratory acceleration of blood from the neck veins. As a result, neck veins become prominently distended during inspiration, a phenomenon referred to as Kussmaul's sign.15



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FIGURE 57-6 Square-root sign in right ventricular pressure tracing in constrictive pericarditis. (Modified with permission from Spodick DH (ed): The Pericardium: A Comprehensive Textbook. Marcel Dekker, New York, 1997; p 4.)

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These pathophysiological entities are all incorporated into the conventional diagnostic criteria for pericardial constriction at cardiac catheterization16:
  1. Equalization of pressures. When pericardial compression is a dominant determinant of hemodynamic status, left and right ventricular end-diastolic pressures are within 5 mm Hg of each other. This classic criterion, however, has a sensitivity of only 60% and a specificity of only 38% for constrictive pericarditis.
  2. Elevation of mean atrial pressures. Mean atrial pressure of over 10 mm Hg is suggestive of either cardiac tamponade or of pericardial constriction.
  3. Square-root sign.
  4. Prominent y descent in right atrial pressure tracing.
  5. Elevated right ventricular end-diastolic pressure. Should be more than one third of right ventricular systolic pressure. This criterion has a sensitivity of 93% and a specificity of 57% for constrictive pericarditis.
  6. Left ventricular ejection fraction. Must be above 40% for a diagnosis of pericardial constriction.

The low sensitivity and specificity of tests make the diagnosis of constrictive pericarditis a difficult one. It is important, however, to distinguish between constrictive pericarditis and other conditions such as restrictive cardiomyopathy because constrictive pericarditis is treatable. The diagnostic criteria for restrictive cardiomyopathy include:

  1. Increased jugular venous pressure
  2. Prominent x and y descents
  3. A small or normal sized heart
  4. Pulmonary congestion
  5. Hepatic congestion
  6. Absence of ventricular hypertrophy or dilatation
  7. Depressed ventricular systolic function

Unfortunately, none of these tests are pathognomonic for restrictive cardiomyopathy. Although noninvasive tests such as echocardiography may qualitatively distinguish normal from thickened pericardium, and may reveal a depressed ejection fraction in the patient suffering from restrictive cardiomyopathy, they too, are not pathognomonic. Invasive hemodynamic monitoring can reveal nuanced differences between restrictive cardiomyopathy and constrictive pericarditis, such as decreased early diastolic filling in restrictive cardiomyopathy but not in pericardial constriction, and divergence in ventricular end-diastolic pressures in restrictive cardiomyopathy but convergence in pericardial constriction after fluid challenge.17 Finally, endomyocardial biopsy may show pathologic change like amyloidosis or fibrosis in patients with restrictive cardiomyopathy, but be normal in the patient with pericardial constriction.18

The low sensitivity and specificity of these tests make it difficult to distinguish between constrictive pericarditis and other conditions such as restrictive cardiomyopathy. In an attempt to increase sensitivity and specificity of tests to diagnose constrictive pericarditis, Hurrell et al measured the respiratory variation of the gradient of left ventricular pressure to pulmonary capillary wedge pressure during the rapid filling of diastole. This was done to assess the dissociation of intrathoracic and intracardiac pressures that is seen in constrictive pericarditis. A difference of 5 mm Hg in the gradient between inspiratory and expiratory cycles had 93% sensitivity and 81% specificity for constrictive pericarditis. Furthermore, increased ventricular interdependence was assessed by comparing left ventricular systolic pressure and right ventricular systolic pressure during respiration. Although concordant increases in left ventricular systolic pressure and right ventricular systolic pressure are expected during inspiration, discordant pressures are encountered during inspiration in patients with constrictive pericarditis. This finding has 100% sensitivity and 95% specificity for constrictive pericarditis.18


?? CONGENITAL ABNORMALITIES
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Most congenital abnormalities of the pericardium are discovered accidentally at cardiac surgery, on routine chest imaging, or while investigating unrelated problems.19 They are rare, and less than 200 cases have been reported in the world literature.20 The rarest of congenital pericardial abnormalities are pericardial bands that obstruct the superior vena cava. The most common are pericardial coelomic cysts.

Partial absence of the pericardium is the most common form of pericardial agenesis. It occurs in approximately 1 out of 14,000 births, and has a male preponderance.20 It is usually associated with cardiac, pulmonary, or skeletal anomalies.20 Most defects tend to occur on the left side, and are due to premature atrophy of the left common cardinal vein, or duct of Cuvier, which normally goes on to form a portion of the left superior intercostal vein. The right duct of Cuvier goes on to form the superior vena cava and ensures closure of the right pleuropericardial membrane.21 Accordingly, right-sided defects tend to be lethal. While complete pericardial agenesis is of little clinical significance, unilateral absence is potentially problematic as it may accentuate cardiac mobility and allow the heart to be displaced into the pleural space with resulting incarceration22 and tricuspid insufficiency.21 The treatment for this lesion is pericardial resection, which may be accomplished thoracoscopically.20 Alternatively, the pericardium can be replaced using patch material via thoracotomy. Both therapies appear to yield good outcomes.

Cysts can occur anywhere on the pericardium, but are found most often in the right costophrenic angle.19 They do not communicate with the pericardial space, and contain a clear yellow fluid. They are typically unilocular, smooth, and less than 3 cm in diameter. Most remain clinically silent, and are discovered on routine chest imaging. Cysts have been associated with chest pain, dyspnea, cough, and arrhythmias probably owing to compression and inflammatory involvement of adjacent structures. They can also become secondarily infected.23,24 Cysts are relatively easy to diagnose by echocardiography or CT imaging, and can be followed in asymptomatic patients. In symptomatic patients, cysts can be aspirated under radiologic guidance, or resected either via the thoracoscope or at thoracotomy.25


?? ACQUIRED ABNORMALITIES
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A large number of factors can cause irritation of the pericardium, inducing the condition known as pericarditis (Table 57-1). The etiologies include myocardial infarction (Dressler's syndrome); drugs such as procainamide and hydralazine; viral, bacterial and fungal infections; metabolic (e.g., uremia) and autoimmune diseases (e.g., rheumatoid arthritis); neoplasms; trauma; and mechanical irritation at the time of surgery. The clinical syndrome in all these cases is similar, and includes pain, constitutional symptoms (such as weakness and malaise), fever (occasionally with rigors), and other symptoms such as cough or odynophagia. The pain is variably described as sharp, dull, aching, or pressure-like. It is generally acute in onset and precordial but can follow referred patterns similar to that of angina, such as to the arm, epigastrium, jaw, shoulder, or ridge of the trapezius. The pain is generally pleuritic, and exacerbated by inspiration, cough, or recumbency. These patients therefore like to sit up and lean forward for relief.


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TABLE 57-1 Acquired etiologies of acute pericarditis

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The cardinal sign of pericarditis is the pericardial rub. Echocardiogram may reveal fibrinous thickening of the pericardium with or without a small effusion. The electrocardiogram may range from normal, to nonspecific ST-segment deviations, to diffuse concave elevation of the ST segments without reciprocal depressions. This may be associated with PR-segment depression, and T-wave inversions in V3 to V6. It should be noted that arrhythmias and conduction abnormalities are not commonly seen in pericarditis, and are suggestive of an underlying cardiac abnormality if present.

After excluding other entities in the differential diagnosis, such as myocardial ischemia, pneumonia, chest wall pain, and pulmonary embolism, treatment should aim to relieve symptoms and eliminate etiologic agents. Nonsteroidal inflammatory drugs (NSAIDs) are the mainstay of treatment,26 and may be supplemented with colchicine.27 Further treatment must be tailored to address the specific etiologic agent, some of which are discussed in greater depth below.

Infectious Pericarditis

Microorganisms may invade the pericardial space from contiguous infections in the heart (e.g., endocarditis), lung, subdiaphragmatic space, or from the wound in postoperative patients. Patients with septicemia can also seed the pericardial space. This problem is more common in immunosuppressed patients.28 Acute surgical intervention is required in the setting of purulent pericarditis, which may result in tamponade in a third of cases,28 or in cases in which scarring results in pericardial constriction.

VIRAL PERICARDITIS

The cardiotropic viruses that cause myocarditis are the ones most likely to cause pericarditis as well. Pericardial inflammation is a result of immune complex deposition, direct viral attack, or both.29 The clinical illness involves pain, friction rub, and typical changes on the electrocardiogram. Treatment is expectant, and symptoms generally resolve with 2 weeks. Surgical intervention is rarely required.

BACTERIAL (SUPPURATIVE) PERICARDITIS

Acute suppurative pericarditis is a life-threatening disease that has the potential to induce tamponade and septicemia. The most common organisms remain streptococcal, pneumococcal, and staphylococcal,30 but the incidence of gram-negative infections such as Escherichia coli, Salmonella, and opportunistic infections is increasing. In adults, pneumopyopericardium is often due to fistula formation between a hollow viscus and the pericardium. However, invasion from contiguous foci, implantation at the time of surgery or trauma, mediastinitis, endocarditis, and subdiaphragmatic abscess can all induce this condition. The clinical course is acute and fulminant. The patient appears toxic and can have a high fever. Aggressive surgical drainage and antibiotic therapy are needed to avoid mortality, which is high.28

TUBERCULOUS PERICARDITIS

After decades of decrease, the incidence of tuberculous pericarditis has been increasing recently because of the rising numbers of immunocompromised patients, particularly those with HIV.31 The pericardium is infected by hematogenous, lymphatic (from lung, bronchial, and mediastinal lymph nodes), peribronchial, or contiguous spread of tuberculosis. The classic pathologic stages of this entity include32:

  1. Fibrinous exudation, with robust polymorphonuclear infiltration
  2. Serous or serosanguinous effusions with a mainly lymphocytic exudation
  3. Absorption of effusion, with organization of caseating granulomas, and pericardial thickening due to fibrin, collagen deposition, and fibrosis
  4. Constrictive scarring, often with extensive calcification

Most often, the clinical course of this entity is insidious. Children and immunocompromised patients may, however, present with a more fulminant course, often demonstrating both constrictive and tamponade physiology.30 The diagnosis is established by examining pericardial fluid for the presence of the mycobacterium. These patients require urgent institution of triple drug therapy. In addition certain groups advocate addition of aggressive surgical management in order to avoid development of chronic constrictive pericarditis.33

FUNGAL PERICARDITIS

Fungal pericarditis is an unusual entity and occurs predominantly in immunocompromised individuals, debilitated individuals, patients with severe burns, infants, and patients taking steroids. Candida and Aspergillus generate an insidious clinical picture, and may come to attention after the patient develops tamponade or constriction. Fungi such as Histoplasma that tend to be endemic to certain geographic areas may cause pericarditis in young, healthy, immunocompetent patients, and will often resolve within 2 weeks. There may be late sequelae such as constriction, but this is rare. Similarly, Coccidioides can also infect young healthy individuals, but will generally produce a more severe illness. Acute pericardial coccidiomycosis usually will accompany pneumonia from the same organism, with systemic adenopathy, osteomyelitis, or meningitis. The potential for chronic constriction is higher in this disease. These conditions all tend to resolve either spontaneously or after treatment with appropriate antifungal medical regimens. Surgical intervention is not usually required in the acute setting.

Metabolic Causes of Pericarditis

Pericarditis has been recognized to occur in the presence of renal failure, hypothyroidism, and autoimmune diseases (such as rheumatoid arthritis), in response to certain drugs (e.g., procainamide and hydralazine), and after mediastinal radiation.

UREMIC PERICARDITIS

Uremic pericarditis was first recognized by Bright in 1836.34 Although it is recognized that nitrogen retention (blood urea nitrogen levels are generally greater than 60 mg/dL) is required for uremic pericarditis, the inciting agent is still unknown. The clinical profile is of a patient with chronic renal insufficiency who has symptoms of pain, fever, and a friction rub. There is usually a pericardial fluid collection, which can be exudative or transudative, and is usually hemorrhagic. The patient may be in tamponade; although the incidence of tamponade is decreasing due to the more widespread use of renal dialysis,35,36 it remains the primary danger of this condition. Management of uremic pericarditis is controversial. Initial therapy includes NSAIDs and aggressive dialysis, and there is also a role for pericardiocentesis or drainage. The timing, however, remains uncertain.37,38 Drainage has been advocated if a pericardial effusion persists despite 2 weeks of aggressive dialysis.39 Any patient with hemodynamic compromise deserves immediate drainage.

DRUG-INDUCED PERICARDITIS

Procainamide (with or without associated lupus syndrome), hydralazine, methysergide, and emetine have all been associated with pericardial inflammation. Minoxidil has been associated with pericardial effusion.40 The clinical presentation and guidelines for management in these settings are similar to those for other conditions. The inciting agent should be discontinued.

PERICARDITIS ASSOCIATED WITH RHEUMATOID ARTHRITIS

Pericarditis is common in patients with rheumatoid arthritis (RA). Approximately half of patients with RA have pericardial effusions, and almost half of all patients with RA have significant pericardial adhesions at autopsy.41 The condition is encountered more often in patients with advanced RA, and is thought to be due to the higher rheumatoid factor titers. The deposition of immune complexes in the pericardium appears to be the inciting event behind the inflammatory response.42 The clinical syndrome varies widely. The most common mode of presentation is a friction rub that lasts days to years with an asymptomatic effusion. The diagnosis is often compounded by the many clinical variants, and by intercurrent diseases such as viral pericarditis and drug-induced pericarditis. Treatment is required only in patients with symptomatic effusions. Constriction may occur late in RA patients. These patients should then be considered for pericardiectomy.

HYPOTHYROIDISM

Severe hypothyroidism produces large, clear, high-protein, high-cholesterol, and high-specific-gravity effusions in 5% to 30% of patients. The effusion may precede other signs of hypothyroidism.43 These effusions are often asymptomatic and are recognized on chest roentgenogram. Clinical tamponade is rare because of the slow accumulation of fluid. However, acute exacerbation due to intercurrent acute pericarditis, hemorrhage, or cholesterol pericarditis can induce cardiac tamponade.44

Radiation Pericarditis

Radiation is the most common etiology of constrictive pericarditis in the United States.45 This was first recognized in patients who received high-dose mantle radiation for Hodgkin's lymphoma in the 1960s and 1970s and later developed cardiac and pericardial diseases. Radiation induces acute pericarditis, pancarditis, and accelerated coronary artery disease in a dose-response fashion.46,47 Cardiac surgery in these patients can be very challenging. Patients may present with a combination of pericardial constriction, restrictive cardiomyopathy, valvular heart disease, and a superimposed ischemic cardiomyopathy. In a large series from Stanford, over 20% of patients with "delayed pericarditis" went on to require surgical pericardiectomy.48

Neoplastic Pericarditis

Secondary neoplasms of the pericardium, that is, tumors that involve the pericardium by metastasis or by infiltration from adjoining structures, account for over 95% of pericardial neoplastic diseases. Rarely, primary pericardial tumors can also arise de novo, and paraneoplastic effusions can also occur that are in response to remote tumors.49

The most common secondary tumors involving the pericardium in males (including both metastasis and local extension) are carcinoma of the lung (31.7%), and esophagus (28.7%) and lymphoma (11.9%). In females, carcinoma of the lung (35.9%), lymphoma (17.0%), and carcinoma of the breast (7.5%) are most common.50 Tumors of the lung, thymus, chest wall, or esophagus are more likely to involve the pericardium by direct spread. Lymphomas, Hodgkin's disease, leukemias, melanomas, and multiple myeloma can infiltrate the pericardium as well as the myocardium. Primary pericardial tumors are rare. Benign tumors are generally encountered in infancy or childhood. Malignant tumors such as mesotheliomas, sarcomas, and angiosarcomas are found in the third or fourth decade of life.51

In both primary and secondary tumor involvement, the clinical presentation is usually silent, and is associated with large pericardial effusions. Tamponade can result if hemorrhage occurs into a malignant effusion. Occasional tumors can induce constriction, due to neoplastic tissue, adhesions, or both. The role of the surgeon is limited to that of a diagnostician in most of these cases.52 Large refractory and tamponading effusions may need to be drained. Pericardiocentesis has a very high failure rate. Subxiphoid drainage or percutaneous balloon pericardiotomy are transiently effective. A pericardioperitoneal shunt may be considered in children. While extensive resection and debulking is desirable in persistent or recurrent malignant pericardial constriction, it is transient without effective adjunctive chemotherapy and/or radiation therapy. In general, life expectancy after malignant pericardial involvement is less than 4 months.53,54

Traumatic Pericardial Disease

PENETRATING TRAUMA

Knives, bullets, needles, intracardiac instrumentation, and cardiac surgery are the most common causes of penetrating trauma to the pericardium.55 Lacerating and penetrating objects like knives cause less physical damage than high-velocity projectiles like bullets. That being said, tamponade is more common in stab wounds than in gunshot wounds. The right ventricle is most commonly involved in anterior chest wounds. Because tamponade provides hemostasis and prevents exsanguination, patients in tamponade appear to have a better survival rate than patients with cardiac stab wounds not in tamponade.56 The corollary of course, is that unless tamponade is released in a timely fashion, it can cause circulatory decompensation and death. Pericardiocentesis has no role in the management of penetrating wounds to the heart. Stable patients can be explored in the operating theater, but unstable patients should undergo thoracotomy in the emergency room.

BLUNT TRAUMA

Blunt injuries to the pericardium rarely occur in isolation. Trauma due to compression, blast, and deceleration will produce a spectrum of injuries, ranging from cardiac contusion to cardiac rupture, and pericardial laceration with herniation or luxation of the heart, which is a surgical emergency. The management of cardiac contusion and cardiac rupture are discussed elsewhere in this book. Here we will focus on pericardial laceration with cardiac herniation. These patients typically suffer deceleration injuries and are invariably hypotensive. They may initially respond to volume resuscitation. A pericardial rub may be the only physical finding, but is not specific for this entity. On chest imaging, free air may be seen in the pericardium, and the heart may be displaced. Intra-abdominal organs may have migrated into the pericardial sac. This is more likely to occur on the left. The immediate management consists of repositioning the patient so as to reduce the herniation. If the heart has herniated into the left pleural space, positioning the patient right-side down may reduce the herniation. Thoracotomy is required for definitive treatment and repair of associated injuries.5759

Peridcarditis Associated with Myocardial Infarction/Dressler Syndrome

This entity is thought to occur in almost half of patients suffering a transmural myocardial infarction, but is discovered in far less.60 Although chest pain is almost universally present, the pain of pericarditis can be distinguished from ischemic pain by its positional and pleuritic nature. The pain of pericarditis tends to start one week after myocardial infarction. A rub is present on auscultation. The electrocardiographic signs of pericarditis are obscured by those of infarction. Patients may develop a small pericardial effusion. Patients suffering from pericarditis appear to have a worse long-term prognosis than those without postinfarct pericarditis,61 possibly because they tend to have larger infarctions as judged by enzyme release and degree of ST-segment elevation. The diagnosis is clinical, and is treated with aspirin and/or NSAIDs.

Cardiac Surgery and the Pericardium

POSTINFARCTION PERICARDITIS

Postinfarction pericarditis may be relevant to the surgeon. To the unwary it may masquerade as postinfarction angina and lead to a needless early operation after a myocardial infarction. Extensive fibrinous adhesions and murky gelatinous fluid may be present in the pericardial space and obscure epicardial vessels. When the pericardium is opened late in such a patient, the surgeon should expect dense pericardial adhesions.

POSTPERICARDIOTOMY SYNDROME

Pericardial friction rubs are almost universal after cardiac surgery, and some patients will develop Dressler's syndrome.62 These patients will almost always respond to a course of NSAIDs, and may occasionally require a short course of corticosteroids. Despite these measures, pericardial effusions may develop in the later postoperative period.

LATE CARDIAC TAMPONADE

Early postoperative tamponade will usually be promptly detected because of a high level of vigilance and close hemodynamic monitoring. It is equally important for surgeons to be aware of the potential for late cardiac tamponade that usually presents after hospital discharge and often initially to a clinician other than the cardiac surgeon. This entity is a potentially lethal complication and occurs in between 0.5% and 6% of patients after heart surgery, almost exclusively in those taking warfarin. Late cardiac tamponade (that is, tamponade occurring more than 7 days after cardiac surgery) is more common in younger patients who have undergone cardiac valve surgery. Patients present on average within 3 weeks of surgery with elevated prothrombin times. They are generally very symptomatic, with declining exercise tolerance, dyspnea, and an inability to diurese, and sometimes hypotension. Although echocardiography will demonstrate a pericardial effusion, the typical echocardigraphic signs of tamponade are detected in only 30% of patients. The diagnosis is therefore a clinical one. Patients respond favorably to pericardiocentesis, and are able to safely resume anticoagulation.63

PERICARDIAL CLOSURE

Surgeons vary in their approach towards closing the pericardium after routine cardiac surgery. Redo sternotomy may be more hazardous when the right ventricle is adherent to the inner table of the sternum. Accordingly, it has been proposed that closing the pericardium at the time of the initial procedure will interpose a protective layer of tissue between the sternum and the heart and thereby reduce the risks of redo sternotomy. The value of this added protection against cardiac injury on sternal reentry is limited by the relative infrequency of reoperation and the low incidence of cardiac injury when the pericardium is left open. On the negative side, closing the pericardium can cause kinking of bypass grafts after coronary bypass surgery and may result in hemodynamic compromise due to cardiac compression. Rao et al demonstrated that pericardial closure at the time of cardiac surgery adversely affects postoperative hemodynamics.64 In this study, the pericardial edges were marked with radiopaque markers and the pericardium was closed with a running suture, the ends of which were exteriorized. After obtaining a postoperative chest film that demonstrated pericardial approximation, a set of baseline hemodynamics were measured. The suture was then removed, another roentgenogram taken to demonstrate that the pericardial edges had become distracted, and then the hemodynamic measurements were repeated. Pericardial closure resulted in transient hemodynamic compromise in the first 8 hours after operation. Conversely, the retrosternal space was significantly larger both 1 week and 3 months after operation (Table 57-2). The risks and benefits of pericardial closure must therefore be weighed against its potential benefits if it is to be used in everyday clinical practice.


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TABLE 57-2 Structural and hemodynamic changes after pericardial closure in patients undergoing elective isolated coronary artery bypass grafting

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?? OPERATIONS
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Mediastinal Reexploration

Standard management for the postoperative cardiac surgical patient involves leaving the pericardium open, and placing anterior and posterior mediastinal thoracostomy drains. Despite this, postoperative tamponade may occur. The typical clinical scenario is one in which chest tube output falls after a period of early postoperative bleeding, the patient develops tachycardia, narrowing of the pulse pressure, increase in right heart filling pressures, decrease in urine output, and a drop in the cardiac index. This setting is diagnostic of tamponade, and arrangements should be made for expedient mediastinal exploration. Echocardiography is not always helpful because the pericardial space is difficult to visualize in the immediate postoperative patient and thrombus is difficult to resolve. Subtle findings that have been reported include an inspiratory increase in right ventricular end-diastolic diameter and a reciprocal decrease in left ventricular diastolic diameter,64 as well as an increase in early peak tricuspid flow velocity and reduction in flow across the mitral valve.65,66

Pericardiocentesis

Pericardiocentesis can be performed at the bedside under local anesthesia in a calm patient, but it is usually performed in the catheterization laboratory. Arterial and right heart catheterization monitoring are frequently used. After administration of 1% lidocaine to the skin and the deeper tissues of the left xiphocostal area, a 25-mL syringe is affixed to a three-way stopcock and then to an 18-gauge spinal needle. This pericardial needle is connected to an ECG "V" lead. Under ECG and fluoroscopic guidance, the needle is advanced from the left of the subxiphoid area aiming toward the left shoulder. A discrete pop may be felt as the needle enters the pericardial space. ST-segment elevation may be seen on the V lead tracing when the needle touches the epicardium. Under these circumstances, the needle is retracted slightly until ST-segment elevation disappears. Once the pericardial space is entered, a guidewire is introduced into the pericardial space through the needle. The needle is removed and a catheter is inserted in the pericardial sac over the guide-wire. At our institution, a pigtail-shaped drainage catheter with an end and multiple side holes is used. Intrapericardial pressure is measured by attaching a pressure transducer system to the intrapericardial catheter. Pericardial fluid may then be removed. When appropriate, samples of pericardial fluid are sent for cell count, chemistry, cytology, cultures, and special stain studies to assist with the diagnosis of the etiology of the effusion. In the presence of pericardial tamponade, aspiration of fluid is continued until there is clear clinical and hemodynamic improvement. If blood is withdrawn, 5mL should be placed on a sponge to see if it clots. Clotting blood suggests that the needle has either inadvertently entered a cardiac chamber or caused epicardial injury. Defibrinated blood that has been present in the pericardial space for even a short time should not clot.67 The catheter is frequently left in place to monitor pericardial fluid drainage. It is secured to the skin with 4-0 silk sutures and covered with a sterile dressing, and the patient is started on prophylactic antibiotics. The pericardial space is drained every 8 hours and the catheter flushed with heparinized solution and in general removed within the next 24 to 72 hours. Pneumothorax is a potential complication, and chest x-ray is mandatory after the procedure.

Pericardial Window

The purpose of partial pericardial resection (window) is to drain fluid into the pleural or peritoneal compartment in order to avoid the reaccumulation of pericardial fluid if the patient has failed prior pericardiocentesis. The procedure can be performed via thoracoscopy, anterior thoracotomy, or subxiphoid incision. General anesthetic is desirable, with the caveat that it may be poorly tolerated in patients with cardiac compression. When the pericardium is encountered, it should be incised. Fluid will invariably drain under pressure. The excised portion of pericardium should be as large as is feasible. Through an anterior thoracotomy, all accessible pericardium ventral to the phrenic nerve should be excised. The surgeon should remain mindful of the rare possibility of cardiac prolapse. Similarly, via the subxiphoid approach, as much diaphragmatic pericardium should be excised as is possible. Thoracostomy drainage catheters should be left within the pericardium.

Pericardial Stripping

Pericardial diseases that produce epicardial or pericardial inflammation (such as radiation or tuberculosis) can cause the pericardium to adhere to the epicardial surface, inducing chronic pericardial constriction. Because of dense adhesions and calcification that can penetrate into the myocardium, pericardial resection can be a technical challenge. The procedure is done via median sternotomy with the capability to go on full cardiopulmonary bypass.18,33 Because of the additional complication of coagulopathy we do not use cardiopulmonary bypass routinely. Left anterior thoracotomy is preferred by some surgeons. The goal of the procedure is to release the ventricles from the densely adherent pericardial shell. The lack of a surgical plane can make this a very bloody operation, and attention must be paid to salvage and reinfusion of blood. Epicardial coronary vessels are at risk in this dissection and particular care must be taken dissecting in these regions. The pericardium should be excised from phrenic nerve to phrenic nerve, and also posteriorly, particularly around the entrance of the vena cavae and pulmonary veins to the pericardium. This complete resection should restore pressure-volume loops to their normal position.68 The results vary with the etiology and severity of the disease. Operative mortality has been reported as high as 10% to 20%69,70 and varies based on severity of heart failure, elevation of right atrial pressure, and comorbidities. Although surgery alleviates or improves symptoms in the vast majority of patients, long-term results are disappointing in patients over the age of 50 and in patients with radiation-induced constrictive pericarditis.13,71


?? ACKNOWLEDGMENTS
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The authors would like to thank Marcia Williams for the preparation of Figure 57-1.


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