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Chylopericardium and cholesterol pericarditis

AUTHOR: Brian D Hoit, MD
SECTION EDITOR: Martin M LeWinter, MD
DEPUTY EDITOR: Susan B Yeon, MD, JD

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Jan 2024.

This topic last updated: Jul 18, 2022.

INTRODUCTION

A pericardial effusion is the accumulation of fluid within the pericardial sac surrounding the
heart that exceeds the small amount that is normally present (typically less than 50 cc).
Pericardial effusion can develop in patients with virtually any condition that affects the
pericardium, including acute pericarditis and a variety of systemic disorders.
Chylopericardium (pericardial effusion composed of chyle) and cholesterol pericarditis
(pericardial inflammation resulting from pericardial effusion with cholesterol crystals and
other inflammatory cells) will be reviewed here. Other causes of pericardial effusion and
pericarditis are discussed separately. (See "Etiology of pericardial disease" and "Pericardial
effusion: Approach to diagnosis", section on 'Identifying the etiology'.)

Chylothorax, with or without chylopericardium, is much more common than isolated

chylopericardium. Most cases are nontraumatic, with the major cause being malignancy,
although inadvertent surgical trauma is also a common cause. Chylothorax is discussed
separately. (See "Etiology, clinical presentation, and diagnosis of chylothorax".)

DEFINITIONS

Chylopericardium is a pericardial effusion comprised of chyle, the normal content of the

lacteals (lymphatics of the small intestine) and thoracic duct ( figure 1). Chylopericardium
may be primary (idiopathic) or, much more often, secondary. The pericardial effusion
appears milky white and opaque, with a triglyceride level greater than 500 mg/dL (5.65
mmol/L) and a cholesterol/triglyceride ratio less than 1.

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Although the cholesterol content is high, chylopericardium should not be confused with
cholesterol pericarditis in which the fluid contains cholesterol crystals, foam cells,
macrophages and giant cells. The fluid in cholesterol pericarditis is clear and classically is
said to have a glittering "gold paint" appearance, although many other colors have been
described [1].

ETIOLOGY

Chylopericardium is a rare disorder that may be primary (ie, idiopathic) or, more often,
secondary to injury to the thoracic duct. The thoracic duct carries chyle from the intestinal
tract to the blood stream ( figure 1). Although wide anatomic variation exists, in most
persons the thoracic duct passes in relatively close proximity to the pericardium over its
course from the cisterna chyli to the jugular and subclavian veins. (See "Etiology, clinical
presentation, and diagnosis of chylothorax".)

Secondary chylopericardium usually results from injury or damage to the thoracic duct. The
most common causes of secondary chylopericardium are:

● Trauma (blunt or penetrating)

● Thoracic or cardiac surgery (especially for congenital heart disease) [2-8]
● Congenital lymphangiomatosis

Other documented causes of secondary chylopericardium include radiotherapy, subclavian

vein thrombosis, infection (eg, tuberculosis), mediastinal neoplasms (eg, lymphoma, signet
ring carcinoma), rheumatologic disease (eg, Behçet syndrome), cystic hygroma, acute
pancreatitis, and Gorham disease [9-12]. (See "Treatment for tenosynovial giant cell tumor
and other benign neoplasms affecting soft tissue and bone", section on 'Gorham disease'.)

Primary or idiopathic chylopericardium is much less common than secondary

chylopericardium and is a diagnosis made by exclusion of other secondary causes [13-18]. In
a systematic PubMed and Wangfang database search for English and Chinese studies
reporting idiopathic chylopericardium from 1950 to 2015, 104 cases from 92 studies were
recovered [19].

CLINICAL MANIFESTATIONS

As with any pericardial effusion, the signs and symptoms related to chylopericardium
depend upon the length of time over which pericardial fluid accumulates and the clinical
situation. The acute leakage of chyle, as would occur following trauma, can result in rapid
pericardial fluid accumulation and increasing intrapericardial pressure resulting in cardiac

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tamponade, while chronic leakage of chyle is typically associated with significant systemic
illness.

The presence of a pericardial effusion may be suspected from the history, physical
examination, electrocardiogram (ECG), and chest radiograph, and confirmed from an
echocardiogram (see "Pericardial effusion: Approach to diagnosis", section on 'Diagnostic
approach'). Clinical features include:

● Most patients without a hemodynamically significant pericardial effusion have no

symptoms specific to the effusion, but they may have symptoms related to the
underlying cause (eg, chest pain and fever in the setting of pericarditis, etc).

● The most common ECG findings in patients with a hemodynamically significant

pericardial effusion are sinus tachycardia, low QRS voltage, and electrical alternans.

● The findings on chest radiograph are variable, depending on the etiology and size of
the effusion and underlying comorbidities. Small to moderate effusions may not result
in significant findings on the chest radiograph, while larger pericardial effusions
typically present with an enlarged cardiac silhouette with clear lung fields.

Significant leakage of chyle causes serious malnutrition, metabolic derangements, and

immunologic incompetence. In addition, cardiac complications can occur including cardiac
tamponade and, since chyle appears to be a pericardial irritant, acute pericarditis or
constrictive pericarditis may also result [1,20]. Rarely, expectoration of chyle (chyloptysis)
may accompany chylopericardium [21].

DIAGNOSIS

The diagnosis of chylopericardium, which may be suspected in patients with a pericardial

effusion and potential trauma or injury to the thoracic duct (see 'Etiology' above), is
confirmed following pericardial fluid analysis. The presence of chylopericardium is suggested
by the discovery of a milky, opaque, and opalescent pericardial effusion during pericardial
fluid sampling, either with pericardiocentesis or surgical pericardial drainage ( picture 1).
The pericardial effusion has a high triglyceride level, with analysis of the fluid typically
revealing [22]:

● Triglyceride level greater than 500 mg/dL (5.65 mmol/L)

● Cholesterol/triglyceride ratio of less than 1
● Negative cultures and cytology
● Lymphocyte predominance on cytologic examination
● Fat globules seen on Sudan 111 staining

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The major cellular component of chyle is the lymphocyte, primarily T lymphocytes. The
lymphocyte count ranges between a few hundred to several thousand per milliliter. The
electrolyte concentration mirrors that of the plasma, and the protein content exceeds 3 g/dL.
The protein content and specific gravity are characteristically high. (See "Pericardial effusion:
Approach to diagnosis", section on 'Identifying the etiology'.)

Contrast-enhanced computerized tomography together with

lymphangiography/lymphangioscintigraphy can be used to help identify an injury or
blockage of the thoracic duct ( image 1) [23]. Scintigraphy after the oral administration of I-
131 triolein has been used to establish the diagnosis in primary chylopericardium [24].

DIFFERENTIAL DIAGNOSIS

The differential diagnosis of a milky white pericardial effusion is limited and generally
includes cholesterol pericarditis and purulent pericardial effusions.

● Cholesterol pericarditis is distinguished from chylopericardium by the presence of

cholesterol crystals and a lower triglyceride concentration. (See 'Cholesterol pericarditis'
below.)

● A purulent pericardial effusion, typically resulting from bacterial or tuberculous

infection involving the pericardium, may also appear whitish on fluid sampling.
However, a purulent effusion is differentiated from chylopericardium by the cellular
content (more neutrophils than lymphocytes), cultures for the causative organism, and
significantly lower triglyceride levels than seen with chylopericardium.

TREATMENT

Initial treatment for chylopericardium depends on the presence or absence of symptoms of

cardiac tamponade as well as the underlying etiology. Patients with symptoms suggesting
cardiac tamponade require urgent fluid removal, while those without symptoms of cardiac
tamponade are initially treated with dietary modifications and sometimes with off-label use
of somatostatin. A low fat diet supplemented with medium chain triglycerides, which are
absorbed by the portal vein rather than the lymphatics, should be initiated [25,26]. Patients
with refractory effusions will require surgical therapy to prevent reaccumulation and cardiac
tamponade, while those with systemic evidence of malnutrition will frequently require
supplemental hyperalimentation. Without treatment, chylopericardium is associated with a
high mortality rate.

Cardiac tamponade or large recurrent effusions — Patients with a symptomatic effusion

or a large uncontrolled effusion (an average daily loss of chyle of 500 mL/day for five days)
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usually require more aggressive therapy. Pericardial drainage can initially be accomplished
by pericardiocentesis or tube pericardiostomy; additional therapy typically includes fluid and
electrolyte replacement and intravenous hyperalimentation (in a malnourished patient who
requires supplemental nutrition). This approach is effective in approximately 55 percent of
cases [27]. Nonoperative therapy is usually unsuccessful when chylopericardium is secondary
to congenital lymphangiomatosis.

Surgical therapy is usually considered if conservative therapy does not reduce pericardial
drainage after 7 to 14 days or if the effusion recurs [22,28]. There is no widely accepted daily
drainage volume of chyle that indicates the need for surgical treatment, although significant
nutritional loss is one criterion. Surgery typically consists of ligation of the thoracic duct and
tributary lymphatics, usually via a thoracic approach, along with either pericardiotomy or
pericardiectomy [22,28]. A transabdominal surgical approach with successful interruption of
the thoracic duct (via ligation or surgical clipping) above the diaphragm has been reported,
as has a right-sided thoracoscopic approach to the thoracic duct [18,29].

In patients in whom aggressive therapy is considered inappropriate, a tube can be placed in

the pericardium at one end and in the peritoneum at the other to drain the chyle away from
the pericardium and into the peritoneal cavity where it can be absorbed [7]. Thoracic duct
embolization has been proposed as a simple and effective alternative [30].

Somatostatin for post-operative chylopericardium — Off-label use of the long-acting

somatostatin analog, octreotide, has been successful in the treatment of postoperative
chylopericardium [31]. The mechanism of action is presumed to be a reduction in chyle
production and thoracic duct flow rate.

Mildly symptomatic or asymptomatic patients — Once the diagnosis has been confirmed
with pericardial fluid sampling (typically associated with drainage of the effusion concurrent
with fluid sampling for laboratory analysis), patients who are otherwise asymptomatic or
only mildly symptomatic can have an initial approach of treatment with dietary modifications
without surgical therapy. The milky opalescence may disappear or decrease with fasting or
dietary modification, but it returns after resuming fat intake. In asymptomatic patients, the
effusion may be controlled by adherence to a diet that is low in fat and high in medium chain
triglycerides [25,26]. In favorable cases, the chylous effusion does not recur after a few
weeks of dietary treatment, presumably because the initiating cause has resolved.

CHOLESTEROL PERICARDITIS

The distinction between chylopericardium and cholesterol pericarditis is analogous to that

between chylothorax and chyliform pleural effusion (pseudochylothorax). Cholesterol
pericarditis is a complication of chronic pericardial effusion or chronic scarring of the

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pericardium and is exacerbated by cholesterol crystals [1]. (See "Etiology, clinical

presentation, and diagnosis of chylothorax".)

Common underlying causes of cholesterol pericarditis include:

● Tuberculous pericarditis (see "Tuberculous pericarditis")

● Rheumatoid pericarditis (see "Pericardial involvement in systemic autoimmune
diseases", section on 'Rheumatoid arthritis')
● Pericardial trauma, a less common cause (see "Post-cardiac injury syndromes")

The clinical manifestations of cholesterol pericarditis are related to the underlying etiology
and are similar to other causes of acute pericarditis. Patients may present with systemic
symptoms such as fever, flu-like symptoms, and leukocytosis. The major clinical
manifestations of pericardial inflammation include pleuritic chest pain, pericardial friction
rub, and electrocardiographic changes (eg, widespread ST elevation or PR depression).
Pericardial thickening may also be seen on imaging studies (eg, echocardiography,
computed tomography, or magnetic resonance imaging), although this is a nonspecific
finding. (See "Acute pericarditis: Clinical presentation and diagnosis", section on 'Clinical
features'.)

As with chylopericardium or any other cause of pericardial effusion, pericardial fluid

sampling is required to make the diagnosis. Cholesterol crystals are characteristic of this
relatively rare disease. When a pericardial effusion is relatively acute, cholesterol remains in
solution. However, when the pericardial effusion is chronic, the normal ability to dissolve
cholesterol is impaired and cholesterol crystals are deposited in the pericardium and
effusion [1]. In contrast to chylopericardium, the fluid is usually clear (although it
occasionally may be cloudy or turbid) and classically is said to have a glittering "gold paint"
appearance, although many other colors have been described [1]. Blood associated with
inflammation is thought to be the source of cholesterol in the pericardial fluid, and evidence
of current or previous hemorrhage is usually evident. The pericardium is thicker than
normal, and its inner surface is lined with plaques and cholesterol deposits. The histologic
findings include fibrosis, inflammatory cells, cholesterol clefts, crystals of variable geometry,
and giant cell granulomata.

The effusions in patients with cholesterol pericarditis tend to be large. The concentration of
cholesterol equals or exceeds that of the blood, often attaining values above 500 mg/dL (13
mmol/L). The pericardial effusion associated with myxedema also has a high cholesterol
concentration, but crystals are usually absent. (See "Clinical manifestations of
hypothyroidism".)

Conservative therapy is rarely effective for cholesterol pericarditis. The optimal therapy is
radical pericardiectomy plus treatment of the underlying cause of chronic recurrent

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pericarditis. Pericardiocentesis is seldom effective over the long-term because the

cholesterol effusions tend to recur and can cause tamponade at any time. This procedure
also fails to address the thick, scarred pericardium and does not prevent the late
development of constrictive pericarditis. (See "Cardiac tamponade" and "Constrictive
pericarditis: Diagnostic evaluation" and "Recurrent pericarditis", section on 'Treatment'.)

SUMMARY AND RECOMMENDATIONS

● Chylopericardium is a pericardial effusion comprised of chyle, the normal content of

the lacteals (lymphatics of the small intestine) and thoracic duct ( figure 1).
Chylopericardium may be primary (idiopathic) or, much more often, secondary to injury
to the thoracic duct (eg, trauma, iatrogenic, malignancy). (See 'Definitions' above.)

● As with any pericardial effusion, the signs and symptoms related to chylopericardium
depend upon the length of time over which pericardial fluid accumulates and the
clinical situation. The acute leakage of chyle, as would occur following trauma, can
result in rapid pericardial fluid accumulation and increasing intrapericardial pressures
resulting in cardiac tamponade, while chronic leakage of chyle is typically associated
with significant systemic illness. (See 'Clinical manifestations' above.)

● The diagnosis of chylopericardium is confirmed following pericardial fluid analysis. The

presence of chylopericardium is suggested by the discovery of a milky opalescent
pericardial effusion during pericardial fluid sampling, either with pericardiocentesis or
surgical pericardial drainage ( picture 1). The pericardial effusion appears milky and
opaque, with other findings including a triglyceride level greater than 500 mg/dL,
cholesterol/triglyceride ratio of less than 1, negative cultures and cytology, lymphocyte
predominance, and fat globules. (See 'Diagnosis' above.)

● Initial treatment for chylopericardium depends on the presence or absence of

symptoms of cardiac tamponade as well as the underlying etiology. Patients with
symptoms suggesting cardiac tamponade require urgent fluid removal, while those
without symptoms of cardiac tamponade are initially treated with dietary modifications
and sometimes with off-label use of somatostatin. A low fat diet supplemented with
medium chain triglycerides, which are absorbed by the portal vein rather than the
lymphatics, should be initiated. Patients with refractory effusions will require surgical
therapy to prevent reaccumulation and cardiac tamponade, while those with systemic
evidence of malnutrition will frequently require supplemental hyperalimentation. (See
'Treatment' above.)

● Cholesterol pericarditis is a clinical entity distinct from chylopericardium in which the

pericardial fluid contains cholesterol crystals, foam cells, macrophages and giant cells.

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The clinical manifestations of cholesterol pericarditis are related to the underlying

etiology and similar to other causes of acute pericarditis. The diagnosis is made
following the identification of cholesterol crystals within the pericardial fluid.
Conservative therapy is rarely effective for cholesterol pericarditis. The optimal therapy
is radical pericardiectomy plus treatment of the underlying cause of chronic recurrent
pericarditis. (See 'Cholesterol pericarditis' above.)

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10. Andrade Santiago J, Robles L, Casimiro C, et al. Chylopericardium of neoplastic aetiology.

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11. Arendt T, Bastian A, Lins M, et al. Chylous cardiac tamponade in acute pancreatitis. Dig
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16. Chan RM, Dodek A. Chylopericardium in a drug addict. Arch Intern Med 1984; 144:1857.

17. Bewick DJ, Johnstone DE, Landrigan PL. Primary chylopericardium associated with
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19. Yu X, Jia N, Ye S, et al. Primary chylopericardium: A case report and literature review. Exp
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21. Luo X, Zhang Z, Wang S, et al. Chyloptysis with chylopericardium, a rare case and mini-
review. BMC Pulm Med 2018; 18:21.
22. Dib C, Tajik AJ, Park S, et al. Chylopericardium in adults: a literature review over the past
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23. Akamatsu H, Amano J, Sakamoto T, Suzuki A. Primary chylopericardium. Ann Thorac

Surg 1994; 58:262.

24. Hamanaka D, Suzuki T, Kawanishi K, et al. Two cases of primary isolated

chylopericardium diagnosed by oral administration of 131I-triolein. Radiat Med 1983;
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25. Jensen GL, Mascioli EA, Meyer LP, et al. Dietary modification of chyle composition in
chylothorax. Gastroenterology 1989; 97:761.

26. Nguyen DM, Shum-Tim D, Dobell AR, Tchervenkov CI. The management of
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27. Chan BB, Murphy MC, Rodgers BM. Management of chylopericardium. J Pediatr Surg
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28. Wurnig PN, Hollaus PH, Ohtsuka T, et al. Thoracoscopic direct clipping of the thoracic
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29. Rivera-Beltrán S, Ortíz VN, Díaz R, Hernández JA. Transabdominal ligation of the thoracic
duct with pericardial-peritoneal shunting in a case of primary idiopathic chylous

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pericardial effusion. J Pediatr Surg 2013; 48:1434.

30. Nadolski GJ, Itkin M. Thoracic duct embolization for nontraumatic chylous effusion:
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31. Szabados E, Toth K, Mezosi E. Use of octreotide in the treatment of chylopericardium.
Heart Lung 2011; 40:574.
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GRAPHICS

Anatomy of the thoracic duct

Course of the thoracic duct. Although wide anatomic variation exists, in most patients (40 to 60
percent), the left thoracic duct ascends from the cisterna chyli, which is a sac located just anterior to
the first or second lumbar vertebra and which receives drainage from the intestinal and two lumbar
lymphatic trunks. The thoracic duct passes through the aortic hiatus of the diaphragm into the
posterior mediastinum continuing cephalad between the aorta and azygos vein until approximately
the level of the fifth thoracic vertebra where it passes behind the esophagus. Below the fifth thoracic
vertebra, the thoracic duct is commonly a dual or plexiform duct but it becomes a single 2 to 3 mm
duct above that level. The thoracic duct continues cephalad adjacent the esophagus passing posterior
to the aortic arch and left subclavian artery. It then arches over the subclavian artery descending to
empty either as a single (50 percent) or multiple lymphatic channels into the left subclavian vein near

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its confluence with the left internal jugular vein. A one-way valve at this location prevents blood from
entering the thoracic duct. The right lymphatic duct drains into the right subclavian vein.

Graphic 57280 Version 9.0

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Milky chylous pericardial fluid

Reproduced by permission from Chan, RMT, Dodek. Arch Intern Med 1984; 144:1857.

Graphic 77602 Version 2.0

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Primary chylopericardium

CT scan from a patient with primary chylopericardium. The thoracic duct (large arrow) is connected to
the pericardial cavity (small arrow heads).

CT: computed tomography.

Reproduced by permission from: Akamatsu H, Amano J, Sakamoto T, Suzuki A. Ann Thorac Surg 1994; 58:262.

Graphic 69482 Version 4.0

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