Most of the effusions after CABG are minor, left-sided,
and regress spontaneously. A small part of pleural effusions become permanent. Patients with pleural
effusion had significantly longer ICU and hospital
stays and experienced higher rates of complications
than those without pleural effusion.[
8]
Yıldırım et al.[9] showed that four of 62 patients
(6.45%) with pleural effusion after cardiac surgery
required toracotomy and decortication operation for
pleural thickening. It suggests the importance of
pleural effusion after cardiac surgery. In addition,
Labidi et al.[8] demonstrated that peripheral arterial
disease, atrial fibrillation, heart failure, and some
anticoagulants may lead to symptomatic pleural
effusion. The authors reported that older patients and
high serum creatinine level patients had symptomatic
pleural effusion. In our study, however, we found no
significant difference in these preoperative parameters
between the patients with major pleural effusion and those with minor or no pleural effusion. Besides,
elective surgeries were significantly less associated with
pleural effusions in Labidi’s[8] study. However, we were
unable to detect any difference in the development of
pleural effusion between elective and urgent patients.
The differences between these two studies can be
explained by the fact that Labidi's study included only
symptomatic or patients requiring an intervention,
while our patients with minimal pleural effusion were
included in the same group with non-effusion patients.
Therefore, some variables of the patients with pleural
effusion might have changed the results in favor of the
group with effusion.
In another study, Light et al.[2] performed chest
radiographs 28 days after surgery and showed a
significantly higher rate of pleural effusions among
patients undergoing either CABG surgery (63%)
or combined CABG and valve surgery (62%) than
those undergoing VR alone (45%). Labidi et al.[8]
concluded that VR was more strongly associated with
postoperative pleural effusions than CABG. However,
we found that there were significantly higher rates
of pleural effusion in CABG and CABG with VR
patients than VR patients alone, similar to the Light’s
study findings (p=0.007). Unlike our study results,
Light’s study included only pure non-effusion patients
in the control group. However, it did not change the
results. In addition, pleural effusion values in CABG
patients may be contributed by TPT length and
pleural trauma. There were five VR patients in the
study group. This may be caused by an inflammatory
response triggered by cardiopulmonary bypass (CPB).
Moreover, in CABG patients whose LIMA or LIMA
with RIMA was used had a high pleural effusion rate
than those whose only saphenous vein was used in
our study. In addition, Hurlbut et al.[5] reported an
incidence of left pleural effusion of 84% for on the
sixth postoperative day following internal mammary
artery (IMA) grafting compared with an incidence
of 47% after saphenous vein grafting. Similarly,
Yıldırım et al.[9] obtained a strong correlation between
pleural effusion and IMA harvesting. There is a
number of studies reporting similar results in the
literature.[5,10] Christakis et al.[11] revealed that there
was no difference in the development of pleural
effusion between the use of mammary and saphenous
vein groups. The causes of pleural effusion may be
atelectasis, impaired lymphatic drainage, decreased
sternal blood supply, and pleurotomy in mammary
artery harvested patients.[6]
Furthermore, Payne et al.[12] found no differences
related to TPT and ACCT between pleural effusion
and without pleural effusion. Similarly, we found
that TPT and ACCT had statistically no effect
on the development of pleural effusion, based
on the logistic regression analysis. Wynne and
Botti[13] showed that use of CPB had clear negative
consequences on postoperative pulmonary function.
They compared CPB patients with other types of
major surgery in terms of pulmonary function and
were found more frequent lung injury and delayed
pulmonary recovery in CPB patients. Extracorporeal
bypass circuit time may also contribute to the
increased complication by causing an inflammatory
response. Therefore, the pulmonary dysfunction is
thought to be due to effects of an acute systemic
and pulmonary inflammatory response commonly
referred to as “pump lung” [14] or “post-pump
syndrome.”[15]
Additionally, there was no difference in the use
of several medications including ASA, ASA with
clopidogrel and ASA with warfarin between patients
with major pleural effusion and minor or no pleural
effusion who were prescribed with variable medication
as such. As a result, antiaggregants and anticoagulants
were shown to have no effect on developing pleural
effusion. On the other hand, pleural effusion was
not found to be less than the patients prescribed with
several diuretics such as furosemide, aldactazide,
furosemide with aldactazide. Therefore, diuretic
treatment which was prescribed to a discharged patient
had no effect on the prevention of pleural effusion.
In conclusion, clinicians should be more alert
to the development of pleural effusion in CABG
patients than VR patients, as CABG and CABG
with VR patients are more potential candidate for
the development of major pleural effusion than VR
patients alone. Major pleural effusion plays also
an important role for mortality and morbidity, as
they are caused by complications such as atelectasis
and empyema in CABG patients. Prevention of
some complications related to major pleural effusion
after cardiac surgery should be considered in some
variables such as mammary artery harvesting.
Declaration of conflicting interests
The authors declared no conflicts of interest with
respect to the authorship and/or publication of this
article.
Funding
The authors received no financial support for the
research and/or authorship of this article.
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