27
Pericardial Diseases
ROGER E. BREITBART
DEFINITION
Pericardial diseases are those that involve the pericardial
membranes and fluid space surrounding the heart. These
diseases include congenital abnormalities, primary inflam-
matory and infectious processes, secondary reactive
processes, and chronic conditions.
The pericardium comprises outer fibrosal and inner
serosal layers. The serosa is actually a collapsed sac that
envelopes the heart and proximal great vessels. The inner-
most layer forms the visceral pericardium or epicardium.
This is continuous via reflections with the outer serosal
layer that is adherent to the outermost fibrosa, forming the
parietal pericardium. The pericardial sac in the normal
adult contains 15 to 35 mL of serous fluid that resides prin-
cipally in a series of pericardial sinuses, the remainder of
the collapsed sac being virtual space.1
This chapter presents an overview of pericardial
conditions pertinent to pediatric practice but it is, of
necessity, not exhaustive. The author has relied heavily on
the comprehensive and authoritative work of Spodick1,2
and other cited references.
ACUTE PERICARDITIS
Acute pericarditis is the most common pericardial disease
encountered in routine clinical practice. There are myriad
causes, some of which are listed in Table 27-1. Most are
idiopathic cases, which, for the most part, are thought to
be viral or postviral.1,2 Whether infectious, postinfectious,
or autoimmune, there is inflammatory infiltration of the peri-
cardial membranes, with (effusive) or without (noneffusive)
accumulation of excess pericardial fluid. Features common
to both effusive and noneffusive pericarditis are presented
in this section whereas those related specifically to clini-
cally significant fluid accumulation and tamponade are
considered in the next. It is beyond the scope of this chap-
ter to address features unique to each underlying cause.
Chest pain is a prominent symptom in many cases of
acute pericarditis, although it is often lacking in the more
indolent or insidious etiologies. When present, the pain
tends to be sharp and precordial, sometimes radiating, worse
with inspiration or cough, and characteristically positional.
Patients are particularly uncomfortable when recumbent
and typically find some relief sitting up and leaning forward.
Fever is common, especially in viral and bacterial pericardi-
tis. On physical examination, patients may appear quite
uncomfortable. In cases of bacterial pericarditis the patient
may be severely ill with systemic signs of sepsis and shock.
There is typically a pericardial friction rub on auscultation;
contrary to some teaching, a rub is often audible even when
there is a large effusion.3
Several tests may aid in the diagnosis of acute pericarditis.
Progressive electrocardiographic abnormalities are patho-
gnomonic, and discrete stages in this progression have been
described.1,2 Early in the disease, there is characteristic
widespread J-point and ST segment elevation in inferior
and anterior leads (Fig. 27-1). PR segments are deflected
in a direction opposite the P wave (i.e., downward in leads
with upright P waves and upward in those with down-
going P waves).4 Later in the disease, J-points return to
baseline, followed by flattening and eventual inversion of
the T waves. It is critical to distinguish pericarditis from
acute coronary syndromes in adult patients presenting with
chest pain.2
459
460 Acquired Heart Disease

TABLE 27–1. Etiologies of Pediatric Acute Pericarditis

and Pericardial Effusion
Idiopathic (probably viral)
Infection
Bacterial
Neisseria meningiditis
Hemophilus influenza
Staphylococcus aureus
Mycobacterium tuberculosis
Borrelia burgdorferi
Other bacteria, including obligate intracellular species
Viral
Coxsackie virus
Cytomegalovirus FIGURE 27–1 Electrocardiogram showing stage I changes
Human immunodeficiency virus pathognomonic of acute pericarditis, including widespread
Other viruses J-point and ST segment elevation and deflection of the PR
Fungal segments in the direction opposite that of the P wave, generally
Candida PR depression with upright P waves.
Other Adapted from Spodick DH. Pericardial diseases. In Braunwald E,
Parasitic Zipes D.P, Libby P [eds]. Heart Disease, 6th ed. Philadelphia:
Toxoplasma gondii
WB Saunders, 2001: 1823, with permission.
Other
Connective tissue disease and vasculitis
Systemic lupus erythematosus inflammation of adjacent epicardial myocardium.5 An
Rheumatoid arthritis elevated white blood cell count may be found in patients
Rheumatic fever
Inflammatory bowel disease with bacterial pericarditis. The erythrocyte sedimentation
Kawasaki disease rate may be elevated, particularly in association with colla-
Other vasculitides and connective tissue syndromes gen vascular diseases. Other tests related to specific diag-
Other etiologies noses (Table 27-1) may be useful when indicated by history
Postpericardiotomy syndrome and physical findings. Analysis of fluid obtained by pericar-
Renal failure, including uremia and chronic dialysis
Malignancy, especially leukemia and lymphoma diocentesis may be diagnostic in cases of malignant,
Graft versus host disease mycobacterial, and other bacterial pericarditis; pericardial
Pneumonia biopsy is rarely informative.6–8
Myxedema The management of acute pericarditis, aside from
Drug, especially mesalamine treatment of the underlying cause where possible, involves
Trauma, including hemopericardium
Extravasation from indwelling central venous catheters, anti-inflammatory therapy to relieve symptoms and accel-
especially in low-birth-weight neonates erate resolution. Nonsteroidal drugs such as ibuprofen are
Other often very effective. Refractory cases may respond to corti-
costeroids. The addition of colchicine has been effective
Adapted from Spodick DH. The Pericardium: A Comprehensive
in anecdotal reports.1,2,9 Therapeutic pericardiocentesis is
Textbook. New York: Marcel Dekker, 1997.
necessary for tamponade and may also be indicated for
otherwise large effusions.
On chest radiograph, the cardiac silhouette may appear
normal or, if there is an appreciable pericardial effusion,
enlarged. Pleural fluid may be present, more often on POSTPERICARDIOTOMY SYNDROME
the left. Other findings, for example pulmonary infiltrates
or a mediastinal mass, may indicate specific etiologies for Postpericardiotomy syndrome is a form of acute peri-
pericarditis. carditis that merits special note because it is frequently
The echocardiogram may have normal findings in nonef- encountered in centers with active pediatric cardiac surgery
fusive acute pericarditis but more typically shows at least programs. It may occur after any cardiac operation includ-
a small collection of pericardial fluid, often localized poste- ing transplantation.10 A similar or identical syndrome devel-
riorly, if not a circumferential effusion (Fig. 27-2). ops in some patients after chest trauma and rarely as a
Screening blood tests are of limited value in most cases complication of transvenous pacing.1,2,11 The precise etiology
of acute pericarditis. A rise in circulating cardiac troponin is unknown and potential immune-mediated pathophysio-
I has been found in 32% of adult patients with viral or logic mechanisms are debated.10,12–14 Patients present 1 week
idiopathic acute pericarditis and may be indicative of to several months after surgery with low-grade fever and
 Pericardial Diseases
A B
FIGURE 27–2 Echocardiogram of a patient with a large, circumferential pericardial effusion (E). A, Apical four chamber view includ-
ing right atrium (RA), left atrium (LA), right ventricle (RV), and left ventricle (LV). B, Parasternal short-axis view.
the typical signs and symptoms of pericardial inflammation
noted in prior sections of this chapter. Cardiac tamponade
may develop.15 Patients may also have findings indicating
associated pleuritis and pleural effusion. Strategies for the
evaluation and management of postpericardiotomy syndrome
are essentially as reviewed above for acute pericarditis,
and below when complicated by tamponade. Nonsteroidal
anti-inflammatory drugs are the mainstay of therapy.
Corticosteroids may hasten recovery but are not effective
for prevention when administered prophylactically.16,17
PERICARDIAL EFFUSION
AND TAMPONADE
Excess pericardial fluid of any volume may accumulate
in acute pericarditis, postpericardiotomy syndrome, or in
any of a number of more chronic conditions associated
with pericardial transudation (see Table 27-1). Pericardial
effusion may have little effect on cardiac function in some
patients, particularly if it accumulates slowly and the peri-
cardium is sufficiently compliant to avoid the development
of high intrapericardial pressure. Importantly, however,
cardiac tamponade may occur in the presence of pericar-
dial effusion, whether large or small. Rapid accumulation
and tamponade are often the rule in hemopericardium
caused by external trauma or iatrogenic cardiac perforation.
In tamponade, increased intrapericardial pressure limits
venous return to the heart and impairs chamber compliance,
resulting in decreased diastolic filling and compromised
cardiac output. Cardiogenic shock and death may ensue,
often precipitously.
461
Depending on the degree of tamponade, patients with
pericardial effusion may have variable dyspnea, tachypnea,
tachycardia, hypotension, poor perfusion, distant heart
sounds, friction rub, jugular venous distention, hepatomegaly,
and/or altered consciousness.18–20 Some children may
have emesis.15 Pulsus paradoxus, defined as a decline is
systolic blood pressure greater than or equal to 10 mm Hg
during inspiration, is a key diagnostic finding indicative of
tamponade physiology (Figs. 27-3 and 27-4). Such respira-
tory variation can be measured conventionally using the
Korotkoff sounds and may be evident on the pulse-oximetry
waveform.21
Electrocardiographic findings may be normal or may
show changes typical of acute pericarditis. In addition,
there may be electrical alternation of the QRS complex
FIGURE 27–3 Brachial artery pressure tracing demonstrating
pulsus paradoxus, with the corresponding electrocardiogram
above. The systolic pressures at end inspiration (IN), 96 mm Hg,
and peak expiration (EX), 114 mm Hg, differ by 18 mm Hg,
which is the size of the pulsus.
Adapted from Spodick DH. The Pericardium: A Comprehensive
Textbook. New York: Marcel Dekker, 1997, with permission.
462
FIGURE 27–4 Physiology of pulsus paradoxus. Responses to
inspiratory reduction of pleural pressure combine to produce
the inspiratory fall in left ventricular output and arterial systolic
pressure.
Adapted from Spodick DH. The Pericardium: A Comprehensive
Textbook. New York: Marcel Dekker, 1997, with permission.
attributed to oscillation of the heart within the effusion.18
There may be diffusely low QRS voltages, reported to be
indicative of tamponade rather than effusion alone.22
On chest radiograph, the cardiac silhouette may appear
enlarged. If there is a large pericardial effusion, the normal
contours of the right and left heart borders may be obscured,
with the heart taking on a more globular or spherical
configuration.
On echocardiography there is typically a circumferential
pericardial effusion. Exaggerated respiratory variation in
transvalvular flows measured by Doppler is a key diagnostic
finding in tamponade. Less specific is diastolic invagination
or collapse of the right atrial and right ventricular free walls
on imaging.23,24
At cardiac catheterization, needed occasionally to confirm
the diagnosis of tamponade, there is elevation of ventricular
pressures throughout diastole and near-equilibration of
atrial and ventricular diastolic pressures.1,2
Signs of tamponade in a patient with a pericardial effusion
represent an indication for urgent or emergent therapeutic
pericardial drainage, either percutaneously or occasionally
by open surgical drainage. Percutaneous needle aspiration,
ideally including insertion of a pericardial catheter over
a guide wire, is typically accomplished via a sub-xiphoid
approach in infants and children with at least 1 cm of
pericardial fluid along the diaphragmatic contour of the
heart.25,26 Ultrasound or fluoroscopic guidance, if available,
is often helpful. Medical management is of only limited
Acquired Heart Disease
value in this setting.1,2 Acute intravascular volume expansion
aids cardiac filling and may be temporarily helpful while
necessary preparations are made to drain the pericardium.
Inotropes and vasoconstrictors are typically ineffective.
Positive pressure ventilation may further compromise
venous return and is to be avoided if possible.
In the absence of tamponade, there are few indications
for therapeutic pericardial drainage.1,2 Very large pericar-
dial effusions may compress significant portions of lung,
with associated dyspnea, and this is relieved with drainage.
Chronic, recurring effusions that are refractory to medical
therapies may in some cases respond to surgical pericar-
diotomy27,28; percutaneous balloon pericardiotomy has also
been reported in children.29 In acute, effusive pericarditis,
diagnostic pericardiocentesis is indicated when the differ-
ential diagnosis includes bacterial infection or malignancy.
CONSTRICTIVE PERICARDITIS
Constrictive pericarditis, rarely described in children,
occurs when cardiac filling is limited by a scarred, fibrotic,
and sometimes calcified pericardium. Typically, the peri-
cardium is thickened and the pericardial space obliterated;
however, pericardial thickness may be normal,30 and peri-
cardial fluid may be present in a syndrome of effusive-
constrictive pericarditis.31 Constriction may develop days
to months after acute pericarditis of any cause, whether
clinically manifest or silent. It is most often idiopathic
and typically becomes chronic, although transient acute
constriction soon after effusive pericarditis is described.1,2,32
Rarely, constrictive pericarditis may develop years after
cardiac surgery.
The symptoms and signs of constrictive pericarditis
may be very mild or severe and generally resemble those
of congestive right heart failure.1,2 Patients may also have
exertional dyspnea to the extent that ventricular filling,
stroke volume, and hence cardiac output cannot increase
adequately. Dyspnea may be exacerbated in the presence
of pleural effusions. On examination, there is typically a
relative sinus tachycardia; atrial fibrillation and other atrial
tachyarrhythmias may ensue due to atrial dilation. Pulsus
paradoxus may be present in effusive-constrictive peri-
carditis. Jugular venous distention is prominent, and there
is often pulsatile hepatomegaly, ascites, and dependent
edema. On cardiac auscultation there may be a diastolic
S3 knock.
Electrocardiographic findings typically show nonspecific
T-wave abnormalities, and there are often low ventricular
voltages and wide P waves. The chest radiograph may show
a dilated SVC, pleural effusions, and, in more chronic cases,
calcium in the pericardium. Computed tomography and
magnetic resonance imaging may demonstrate a thickened
 Pericardial Diseases
A B
FIGURE 27–5 Magnetic resonance images of a patient with a constrictive pericardium (arrows) encasing the right (RV) and left (LV)
ventricles. A, Parasagittal cut. B, Axial cut.
pericardium (Fig. 27-5) and enlarged atria and venae
cavae.33 Echocardiography may show pericardial thicken-
ing whereas Doppler analysis reveals characteristic abnor-
malities of mitral and tricuspid inflow and ventricular
filling.1,2,23 Cardiac catheterization is necessary to distin-
guish constrictive physiology from that associated with
restrictive cardiomyopathy. Both exhibit the characteristic
square root sign in the ventricular pressure tracings,
reflecting an acute pressure fall at the onset of diastole and
rapid rise in early diastole followed by a plateau (Fig. 27-6).
In restrictive disease, however, the left ventricular diastolic
pressure exceeds that of the right, accentuated by fluid
challenge, whereas in constrictive disease they are nearly
equal.
Surgical pericardiectomy is required to treat constrictive
pericarditis as medical management is ineffective.1,2,34
CONGENITAL PARTIAL OR COMPLETE
ABSENCE OF THE PERICARDIUM
Absence of the pericardium is a rare malformation in
which the pericardium is incomplete, in part or in total,
presumably the result of defective embryonic development.
When such defects occur, it is the left side of the pericardium
that is most often absent, whereas absence of the right
463
pericardium is less common. Absence of the inferior peri-
cardium is associated with diaphragmatic defects. Complete
absence of the pericardium is exceedingly rare.1,2 A family
with absence of the left pericardium has been described.35
Absence of the pericardium is most often clinically silent
but may become manifest, particularly in partial absence,
when there is herniation, incarceration, or torsion of
critical cardiovascular structures including the atria, atrial
appendages, ventricles, and great vessels, impairing cardiac
filling and output.36 Rupture of tricuspid valve chordae has
been reported.37 Compression of the epicardial coronary
vessels can produce atypical angina pectoris and myocardial
infarction.38,39
The clinical presentation is variable.40 Some patients may
have paroxysmal chest pain but most are asymptomatic.
Findings on physical examination and electrocardiogram
may be absent or nonspecific.41 Displacement of cardiac
structures, mainly left lateral displacement of the apex,
may be recognized on plain chest radiograph (Fig. 27-7A)
and particularly exaggerated on decubitus films.42
Echocardiography may show unusual acoustical windows
and abnormal cardiac and septal motion.43 Magnetic reso-
nance imaging is the definitive modality for delineating the
precise anatomy (Fig. 27-7B).44
Management of symptomatic patients may involve
surgical reconstruction of the defective pericardium using
 A B C
FIGURE 27–6 Intracardiac pressure recordings in constrictive pericarditis. A, Left ventricular pressure tracing, with corresponding
electrocardiogram above, demonstrating the square root sign with dip and rapid rise in early diastole. Reprinted with permission from
Spodick DH. The pericardium: A comprehensive textbook. New York Marcel Dekker, 1997. B,C, Simultaneous pressure tracings from a
patient with constrictive pericarditis showing equalization of left ventricular (LV), right atrial (RA), and right ventricular (RV) diastolic
filling pressures.

A B
FIGURE 27–7 Images of a patient with congenital absence of the left pericardium. A, Chest radiograph showing leftward displacement
of the cardiac apex. B, Magnetic resonance image showing that the pericardium (P) is absent posterolaterally (arrows) around the left
ventricle (LV) in an axial cut.
 Pericardial Diseases
synthetic or xenograft membrane or, alternatively, partial
pericardiectomy to enlarge small incarcerating defects.39,40
PERICARDIAL CYSTS AND TUMORS
Isolated, fluid-filled pericardial cysts of several types
may be found at any location on the pericardium, usually
incidentally.1 If large, however, they can produce symp-
toms by compression of the heart, mimicking tamponade,
or of other adjacent structures. They must be differenti-
ated from other cystic mediastinal masses with the aid of
computed tomography, echocardiography, or magnetic
resonance imaging. Treatment, if necessary, may involve
aspiration or excision.45
Primary pericardial tumors are exceedingly rare.
Teratoma,46 lipoma, 47 hibernoma,48 and mesothelioma49
have been reported.
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