Pleural Effusions Following Cardiac Injury and Coronary Artery

Pleural Effusions Following Cardiac Injury
and Coronary Artery Bypass Graft Surgery
Richard W. Light, M.D.1,2
This article discusses the pleural effusions that occur with the post–cardiac injury (Dressler’s) syndrome (PCIS) and those that occur after coronary artery bypass graft
(CABG) surgery. The PCIS can occur after any type of cardiac injury and is thought to
be due to antimyocardial antibodies. The primary symptoms are fever and chest pain, and
pericarditis is frequently present. Pleural effusions are common with PCIS. The primary
treatment for PCIS is a nonsteroidal anti-inflammatory agent or corticosteroids. Following CABG surgery, most patients will have a small unilateral left-sided pleural effusion,
and approximately 10% of patients will have a larger effusion. These large effusions can be
separated into early effusions occurring within the first 30 days of surgery that are bloody
exudates with a high percentage of eosinophils, and late effusions occurring more than
30 days after surgery that are clear yellow lymphocytic exudates. The primary symptom of
a patient with a pleural effusion post–CABG surgery is dyspnea; chest pain and fever are
uncommon. Most patients with large pleural effusions postCABG surgery are managed
successfully with one to three therapeutic thoracenteses.
KEYWORDS: Pleural effusion, CABG surgery, postcardiac injury syndrome
Objectives: Upon completion of this article, the reader should understand the etiology, diagnosis, and management of the
post–cardiac injury syndrome and the pleural effusions that occur after coronary artery bypass surgery.
Accreditation: The University of Michigan is accredited by the Accreditation Council for Continuing Medical Education to sponsor
continuing medical education for physicians.
Credits: The University of Michigan designates this educational activity for a maximum of 1.0 hour in category one credits toward
the AMA Physicians Recognition Award.
The post–cardiac injury syndrome (PCIS) is characterized by the development of fever, pleuropericarditis,
and parenchymal pulmonary infiltrates in the weeks
following trauma to the pericardium or myocardium.1,2 In a recent article, noncomplicated post–
cardiac injury syndrome was defined as the presence of
temperature > 100.5°F, patient irritability, pericardial
friction rub, and a small pericardial effusion with or
without pleural effusion following cardiac trauma.3
These same authors defined a complicated PCIS as a
noncomplicated PCIS plus the need for hospital readmission with or without the need for pericardiocentesis or thoracentesis.3 PCIS has been reported following myocardial infarction, cardiac surgery, blunt chest
trauma, percutaneous left ventricular puncture, pacemaker implantation, and angioplasty.
Seminars in Respiratory and Critical Care Medicine, volume 22, number 6, 2001. Address for correspondence and reprint requests: Richard W.
Light, M.D., Saint Thomas Hospital, 4220 Harding Rd., Nashville, TN 37205. E-Mail: 1Saint Thomas Hospital,
Nashville, Tennessee; 2Vanderbilt University, Nashville, Tennessee. Copyright © 2001 by Thieme Medical Publishers, Inc., 333 Seventh Avenue,
New York, NY 10001, USA. Tel: +1(212) 584-4662. 1069-3424,p;2001,22,06,657,664,ftx,en;srm00117x.
The incidence of PCIS has varied markedly from series
to series. The explanation is obvious when the above
mentioned definition is used. If one evaluates patients
critically, most patients with cardiac trauma will meet
the criteria for uncomplicated PCIS. Most patients
post–cardiac trauma will have evidence of a systemic inflammatory response as evidenced by increased serum
levels of interleukin-6 (IL-6).4 Probably there is a continuum of responses post–cardiac trauma ranging from
mild fever and chest soreness to the complete Dressler’s
syndrome with fever, pleuritic chest pain, pleural effusion, pericardial effusion, and parenchymal infiltrates.
When Dressler first described the syndrome following myocardial infarction, he stated that the incidence was 3 to 4%.1 Subsequent articles have indicated
that the incidence is less than 1% following myocardial
infarction.5 However, if the patient has pericarditis in
the few days following the myocardial infarction, then
the incidence of PCIS is approximately 15%.6 In recent
years the incidence of PCIS after myocardial infarction
has decreased to less than 0.5%. This has been attributed to the increased use of thrombolytics resulting in
early reperfusion and less tissue damage.7
The reported incidence of PCIS following cardiac surgery has varied from 153 to 30%.2 In a recent series of 266 children undergoing cardiac surgery, the incidence of uncomplicated PCIS was 11.2%, whereas the
incidence of complicated PCIS was only 3.4%.3 In an
older series of 966 adults undergoing cardiac surgery at
Johns Hopkins Hospital, the incidence of PCIS was
17.8%.8 To be classified as having the PCIS in this series, patients were required to have two or three of the
following signs and symptoms during their hospitalization or follow-up visit: (1) fever greater than 37.8°C,
(2) significant anterior chest pain suggestive of pericardial inflammation, and (3) a two- or three-component
pericardial friction rub on auscultation.8 The incidence
of PCIS was comparable after all types of cardiac surgery. However, there was a higher incidence of PCIS if
the patient had a history of pericarditis or if the patient
had taken corticosteroids previously.8
The etiology of the PCIS is not completely known, but
it appears to have an immunologic basis. When the
myocardium is injured, cellular components, including
autoantigens, are released. These autoantigens can provoke an autoimmune antibody reaction by antimyocardial antibodies. Subsequently, complement is activated,
C3 and C4 levels fall, and leukocytes are mobilized.
There is a close relationship between the occurrence of PCIS and the development of antimyocardial
antibodies in patients undergoing surgical procedures
involving the pericardium. In one prospective study of
257 patients, 67 patients (26%) developed high titers of
antimyocardial antibodies, and all 67 developed PCIS.2
In contrast, none of 102 patients without a rise in antibody titers and only 4 of 93 patients with intermediate
titers developed the syndrome.2 There is not a clear-cut
relationship between the development of antimyocardial antibodies and PCIS in patients with myocardial
infarction. In one study of 136 patients with myocardial
infarction, there was no association between the development of the syndrome and the presence of antimyocardial antibodies.5
Epidemiological studies have indicated that
there are other factors that appear to be associated with
the development of the post–cardiac injury syndrome.
There is a seasonal variation in the post-cardiac injury
syndrome, with the highest incidence corresponding to
the time of the highest prevalence of viral infection in
the community.9 De Scheerder and coworkers have hypothesized that a concurrent viral infection may trigger
the immune response.10
Clinical Manifestations
The clinical manifestations of PCIS include fever, chest
pain, pericarditis, pleuritis, and/or pneumonitis. As commented upon previously in this article, however, many
patients are given the diagnosis of PCIS with only two of
the five manifestations. Following myocardial infarction,
the symptoms usually develop in the second or third
week; an occasional patient develops symptoms within
the first week, whereas a larger percentage develop symptoms only after the third week.11 Following cardiac surgery, the syndrome is seen at an average of 3 weeks but
can occur any time between 3 days and 1 year.12
The two cardinal symptoms of PCIS are chest
pain and fever. The chest pain often precedes the onset
of fever and varies from crushing and agonizing, mimicking myocardial ischemia, to a dull ache to pleuritic chest
pain. A pericardial friction rub is present in almost all
patients and a pericardial effusion is present in the majority. Laboratory evaluation reveals a peripheral leukocytosis and an elevated erythrocyte sedimentation rate
(> 100 mm/hr) in most patients.2,13 The chest radiograph reveals pulmonary infiltrates in the majority of
patients.13 Approximately 80% of the patients will have
a pleural effusion, and the effusions are bilateral in approximately 50%.13 When the effusions are unilateral,
they are more commonly on the left than on the right.
The pleural fluid is an exudate with a normal pH and a
normal glucose level.13 The pleural fluid is frankly
bloody in about 30% of patients, and the differential cell
count may reveal predominantly polymorphonuclear
leukocytes or mononuclear cells depending upon the
acuteness of the process.13
The diagnosis of PCIS should be considered in any patient who develops a pleural effusion following trauma
to the heart and who is febrile and has chest pain. Since
there are no specific tests with which to establish the
diagnosis, the diagnosis is made by excluding other
diseases that can produce identical symptoms in the
patient post–cardiac injury. The main diagnoses to exclude are pleural effusions post–coronary artery bypass
(CABG) surgery, congestive heart failure, pulmonary
embolism, and pneumonia with a parapneumonic effusion or empyema.14 Pleural effusions due to PCIS and
those due to CABG surgery are distinguished primarily
by the patient’s symptoms; patients with pleural effusions due to PCIS invariably have chest pain and fever,
whereas those with pleural effusions post–CABG surgery have dyspnea, but no chest pain or fever. Congestive heart failure is excluded if the pleural fluid is an exudate. The possibility of pulmonary embolism can be
evaluated with a spiral computed tomography (CT)
scan or with a perfusion lung scan. It is important not to
mistakenly diagnose the PCIS as a pulmonary embolism. Anticoagulation is contraindicated with the
PCIS syndrome because patients with the syndrome are
at risk for developing hemopericardium and tamponade.15 The possibility of pneumonia is high if the patient has purulent sputum, and the diagnosis of pleural
space infection is established if the pleural fluid cultures
are positive or the pleural fluid is purulent. One report
suggested that the diagnosis of the syndrome could be
established by demonstrating a high titer of antimyocardial antibody and a low complement level in the
pleural fluid.16
Prevention and Treatment
There is no known means by which to prevent the development of PCIS. Mott and coworkers3 randomized 246
children who were undergoing cardiac surgery with cardiopulmonary bypass to receive intravenous methylprednisolone (1 mg/kg) or saline prior to cardiopulmonary
bypass and q 6 hours for four doses post-surgery. They
found that the incidence of PCIS was identical in the
two groups. Possibly a different result would have been
obtained if the corticosteroids had been given for a
longer duration.
Once the syndrome has developed, it usually responds to treatment with anti-inflammatory agents
such as aspirin or indomethacin. My choice is indomethacin 25 to 50 mg every 8 hours. Although a single
episode of the PCIS is usually self-limited, recurrences
are frequent. Recurrent episodes become progressively
more resistant to treatment with nonsteroidal antiinflammatory agents, but usually respond to corticosteroid therapy.17 Prednisone is administered orally in doses
of 40 to 60 mg daily with rapid tapering over 8 to
10 days.17 If symptoms recur when the prednisone is tapered, additional courses are indicated.
One report suggested that the development of
the PCIS postoperatively in patients who had undergone CABG surgery was a very serious event because
the grafts were likely to be occluded by the inflammatory process.12 When 31 subsequent patients were
treated with prednisone, 30 mg per day for a week and
tapering doses for 5 weeks thereafter, in addition to aspirin 600 mg qid, only 16% of the grafts became occluded.12 However, it should be noted that this report
has not been validated since it was originally published
in 1976.
More than 600,000 patients undergo CABG surgery in
the United States each year.18 Given that approximately
10% of the patients who undergo CABG surgery will
develop a pleural effusion occupying more than 25% of
the hemithorax in the subsequent month,19 CABG surgery is one of the more common causes of pleural effusions in the United States.
Many patients who undergo CABG surgery will develop a small, left-sided pleural effusion in the first few
days postoperatively. In one study of 122 patients, the
incidence of pleural effusion on the routine chest radiograph 6 days postoperatively was 42%.20 In this study,
the incidence of pleural effusion was nearly identical in
patients who received internal mammary artery (IMA)
graphs (43%) and in those that received only saphenous
vein grafts (SVG) (41%).20 Approximately 80% of the
effusions in this series were small (occupying less than
one intercostal space) and were unilateral left-sided.20
In a second study the same investigators performed
chest ultrasound at 7, 14, and 30 days postoperatively on
47 patients and reported that the prevalence of pleural
effusion was 89% at 7 days, 77% at 14 days, and 57% at
30 days.21 The higher incidence of effusion in this latter
series was attributed to the increased sensitivity of ultrasound as compared with the chest radiograph at detecting pleural fluid. The majority of the pleural effusions
were unilateral and left sided in this series. In contrast
to the previous study, the prevalence of pleural effusions
was higher in this series if the patients received an IMA
graft.21 In a third study, Landymore and Howell reported that at the time of discharge from the hospital,
the incidence of pleural effusion was 91% in 34 patients
who had received an IMA graft and had the pleura
opened, whereas the incidence of pleural effusion was
58% in 33 patients who had received an IMA graft but
in whom the pleura was not opened.22
The natural history for the small, unilateral, leftsided effusions is gradual resolution.21,22 However, in
certain patients, the effusion enlarges and produces
symptoms. Hurlbut and associates23 obtained chest radiographs 8 weeks postoperatively on 76 patients who
had received IMA grafts and reported that 5 of 55 patients (9.1%) who underwent pleurotomy and 3 of
21 patients (14.5%) who had an IMA without pleurotomy had a pleural effusion at the 8-week follow-up
visit. Four of these 76 patients underwent thoracentesis.
In a recent prospective study from our institution,19 the
prevalence of pleural effusions at approximately 30 days
post-operatively on chest radiographs in 349 patients
who had undergone CABG surgery was 63%. Although
most of the effusions were small, 34 of the 349 patients
(9.7%) had a pleural effusion that occupied more than
25% of the hemithorax. The incidence of large effusions
was higher in the 282 patients who received an IMA
graph (10.9%) than in the 67 patients that received only
SVG graphs (4.5%).
The pathogenesis of the pleural effusions following
CABG surgery is not definitely known. The early,
small, left-sided effusions are probably related to the
trauma of surgery including phrenic nerve injury and
atelectasis. Large effusions (those occupying more than
25% of the hemithorax) can be divided into two categories: those occurring within the first 30 days and
those occurring after the first 30 days.24,25 The early effusions are usually bloody with a median hematocrit
above 5%. The likely etiology of these effusions is
trauma from the surgery and postoperative bleeding
into the pleural space.25
The etiology of the effusions occurring later is
unclear. These effusions tend to be clear with a predominance of lymphocytes in the pleural fluid.24,25 It has
been suggested that these effusions are manifestations
of the PCIS.26 However, it is unlikely that these effusions represent the PCIS because the two main clinical
manifestations of the PCIS are chest pain and fever3;
both symptoms are very uncommon in patients with
pleural effusions more than 30 days after surgery.19
The observation that the pleural fluid associated
with the late effusions post–CABG is lymphocytic suggests an immunological etiology. To my knowledge
there have been no studies of the serum levels of antimyocardial or antimesothelial cell antibodies in these
individuals. Antimyocardial antibody was detected in
the pleural fluid and in the serum of one patient with a
pleural effusion secondary to PCIS post–CABG surgery. However, we could detect no antimyocardial antibody in the pleural fluid of 25 patients with pleural ef-
fusions post-CABG (unpublished observations) who
did not have fever and chest pain.
When pleural specimens from patients undergoing thoracoscopy for persistent post-CABG pleural effusions are examined, there is an intense lymphocytic
pleuritis with little fibrosis within the first few months
of surgery (Fig. 1).27 Immunohistochemical analysis
demonstrates that there is a mixed population of lymphocytes with a predominance of B cells.27 As time goes
on, there is a gradual decrease in the cellular infiltrate
and a gradual increase in the degree of fibrosis.27 After
1 year or more, the pleura is markedly thickened with
increased amounts of dense fibrous tissue (Fig. 2). The
fibrous component is typically paucicellular, but it does
contain collections of entrapped cells that are cytokeratin immunoreactive, compatible with mesothelial
The occurrence of pleural effusions post–CABG
surgery is increased if the patient receives topical hypothermia at the time of surgery with iced slush. Nikas
and coworkers studied 505 nonrandomized consecutive
patients undergoing CABG surgery and reported that
60% of the 191 patients who received topical hypothermia had a pleural effusion, whereas only 25% of the
314 patients who did not receive topical hypothermia
developed a pleural effusion.28 Moreover, 25% of those
in the hypothermia group required a thoracentesis,
whereas only 8% of those in the control group required
a thoracentesis.28 In a second study, Allen and associates
reported that the incidence of pleural effusion was 50%
in 50 patients who received topical hypothermia but
only 18% in 50 patients who did not receive topical hypothermia.29 These data suggest that cold injury to the
phrenic nerve resulting in atelectasis may cause the
pleural effusion.
As mentioned previously, patients who receive an
IMA graft are more likely to develop a large pleural effusion than are those who receive only SVG. In addi-
Figure 1 Pleural specimen from a patient 3 months post–
coronary artery bypass graft (CABG) surgery with a persistent
pleural effusion. Note the intense lymphocytic pleuritis.
Figure 2 Pleural specimen from a patient 12 months post–
coronary artery bypass graft (CABG) surgery with a persistent
pleural effusion. Note the dense fibrous tissue.
tion, the type of chest drain used postoperatively
may influence the development of pleural effusions.
Robinowitz-Elins and associates reported that a thoracentesis was required in only 2 of 295 patients (1%) who
received a Blake Drain (19F) postoperatively compared
with 48 of 1547 (3.1%) who received a conventional
chest tube (32F).30 We recently reported that patients
who underwent CABG surgery off pump (without cardiopulmonary bypass) had a lower incidence of large
pleural effusion 4 weeks postoperatively than did those
who underwent CABG surgery with cardiopulmonary
Clinical Manifestations
The primary symptom of patients with pleural effusion
post–CABG is dyspnea. In a recent study from our institution, 22 of 29 patients (75.9%) with an effusion occupying more than 25% of the hemithorax complained
of dyspnea, but only 3 (10.3%) complained of chest pain
and only 1 (3.4%) complained of fever.19 It should be
noted that almost every patient with the PCIS syndrome has both chest pain and fever.
The pleural effusions that occur after CABG
surgery tend to be unilateral on the left side. In the
study from our institution in which chest radiographs
were obtained approximately 4 weeks post-surgery,
196 of 349 patients (62%) had pleural effusions.19 The
effusions were unilateral or larger on the left in
155 (73.4%), whereas they were unilateral on the right
or larger on the right in only 14 (7.2%).19
As mentioned previously, the larger pleural effusions that occur after CABG can be divided into those
that occur within the first 30 days of surgery and those
that occur more than 30 days after surgery.25,26 The
pleural fluid from the early effusions is bloody with a
median red blood cell count of > 700,000 cells mm3
(Table 1).25 The pleural fluid is frequently eosinophilic
with median eosinophil percentage of nearly 40.25 The
median pleural fluid lactate acid dehydrogenase (LDH)
level is approximately twice the upper limit of normal
for serum.25 Because the pleural fluid is bloody, it is
likely that the LDH in the pleural fluid is LDH-1,
which is the LDH from the red blood cells. The pleural
fluid protein is in the exudative range, and the pleural
fluid glucose is not reduced.25
The pleural fluid from the late-appearing pleural
effusions is quite different from the bloody fluid with
the high eosinophil count and the high LDH level seen
in the early effusions. The fluid from the late effusions
is usually a clear yellow exudate that contains predominantly lymphocytes. In one series the median lymphocyte percentage in 26 pleural fluids from late effusions
was 68%, whereas the median eosinophil percentage
was 0.25 The median level of LDH is approximately the
upper normal limit for serum. The pleural fluid protein
is in the exudative range, and the pleural fluid glucose is
not reduced.25 The pleural fluid adenosine deaminase is
below 40 IU/L.32
Table 1 Comparison of the Characteristics of the Pleural Fluid in Patients with the PCIS
Syndrome, Early Effusions Post–CABG Surgery and Late Effusions Post–CABG Surgery
Early Post–CABG
Late Post–CABG
Clear Yellow
Bloody or
PMNs or
Mononuclear cells
Exudative range
Exudative range
High titer
Neutrophils and
Exudative range
2 upper limit
Exudative range
1 upper limit
Differential WBC
When a patient is seen with a pleural effusion post–
CABG surgery, there are several other diagnoses to
consider in addition to the pleural effusion secondary to
CABG surgery. The main diagnoses to exclude are congestive heart failure, pulmonary embolus, parapneumonic effusions, the PCIS, and chylothorax.14 The
work-up of the patient is influenced by the patient’s
symptoms. If the patient is asymptomatic and the effusion is predominantly left-sided and occupies less than
25% of the hemithorax, it can be attributed to the coronary artery surgery without performing a thoracentesis.
If the patient is febrile or has chest pain, a thoracentesis
should be performed to rule out a pleural infection. In
this situation, consideration should also be given to the
possibility of a pulmonary embolism. If dyspnea is out
of proportion to the size of the effusion, the possibility
of a pulmonary embolism should also be considered. If
the effusion is large, the patient should undergo a therapeutic thoracentesis to verify that a chylothorax is not
present and to alleviate dyspnea if the patient is dyspneic. If the effusion is a late effusion with lymphocytes
predominating in the pleural fluid, the diagnosis of tuberculosis should be excluded. This is most easily done
by measuring the level of ADA (adenosine deaminase)
in the pleural fluid since the pleural fluid ADA level is
almost always above 40 with tuberculous pleuritis but is
almost always less than 40 with the pleural effusion
post–CABG surgery.32
There are no controlled studies that address the treatment of the pleural effusion due to CABG surgery. If
the effusion is small and the patient is asymptomatic,
no treatment is necessary because such effusions virtually always resolve. If the effusion is larger and the
patient is symptomatic, a therapeutic thoracentesis
should be performed. If a symptomatic effusion recurs
after the initial therapeutic thoracentesis, a second
therapeutic thoracentesis should be considered. If the
effusion recurs, many patients are also given nonsteroidal anti-inflammatory agents or prednisone, but
there are no controlled studies documenting the efficacy of this approach. In like manner, chemical pleurodesis has been successful in some patients. It is important to realize that the great majority of patients
with large pleural effusions will do well with only therapeutic thoracentesis. In our prospective study, we followed 30 patients who had a pleural effusion occupying
more than 25% of their hemithorax for 12 months.
Eight of the patients (27%) received no invasive treatment for their pleural effusion, 16 (53%) were treated
with a single therapeutic thoracentesis, 2 (7%) required
two thoracenteses, and 4 (13%) required three or more
thoracenteses.19 One patient was still receiving periodic
thoracentesis 12 months post-CABG.
In rare instances, the patient continues to be
symptomatic despite several thoracenteses. Over the
past few years we have subjected eight such patients to
thoracoscopy. At thoracoscopy, several patients had thin
sheets of fibrous tissued that coated the lung and prevented it from expanding.27 We hypothesize that this
sheet of fibrous tissue “trapped” the lung and prevented
it from reexpanding (Fig. 3). The incidence of trapped
lung after CABG surgery is not known, but is probably
very low. At our hospital, where 2500 CABG surgeries are performed annually, only four case of trapped
lung were seen during a recent 2-year period.27 The diagnosis of trapped lung can be established by measuring
Figure 3 (A) Posterioanterior chest radiograph demonstrating a moderate-sized left pleural effusion in a patient who was 4 months
post–coronary artery bypass graft (CABG) surgery. (B) Chest computed tomographic scan with contrast of the patient in Figure 3A
demonstrating a loculated left pleural effusion with thickening of the visceral pleural. At thoracoscopy this patient was found to have
a thin sheet of fibrous tissue covering the visceral pleural. Decortication resulted in resolution of the pleural effusion.
the pleural pressure as fluid is withdrawn. If the pleural
pressure is initially below 10 cm H2O or if the pleural
pressure falls more than 20 cm H2O per 1000 mL fluid
removed, the diagnosis is strongly supported.33 After
the fibrous tissue coating the visceral pleural was removed, the lung expanded, and the effusion did not
recur. However, given that most of the patients had a
mechanical or a chemical pleurodesis at the time of thoracoscopy, it is not clear that the decortication itself was
responsible for the resolution of the pleural effusion.27
Thoracoscopy is recommended for an effusion
after CABG that continues to recur for several months
despite several therapeutic thoracenteses. At thoracoscopy, any fibrous tissue coating the visceral pleura
should be removed and the parietal pleura should be
abraded to create a pleurodesis.
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