Background: More than 85% of patients develop pleural effusions after coron
ary artery bypass grafting (CABG). Although the majority resolve spontaneou
sly, post-CABG effusions carl persist. The cause of these persistent effusi
ons is unknown, and the histology of the pleural changes has seldom been re
ported.
Objectives: To describe the patient characteristics and pathologic conditio
n of the pleural tissues in patients with persistent post-CABG effusions.
Subjects: Eight patients with persistent post-CABG effusions who underwent
thoracoscopy or thoracotomy over a 2-year period by one thoracic surgeon. T
hese eight patients were selected as having undergone CABG > 2 months befor
e their thoracic surgery and had no other identifiable causes of effusion.
Results: The median time from CABG to pleural surgery was 132 days (range,
74 to 2,258 days). The median left ventricular ejection fraction was 57% (r
ange, 15 to 70%). All patients were dyspneic and had large (greater than or
equal to 25% of the hemithorax) effusions on chest radiograph. All effusio
ns persisted after two or more thoracenteses. Pleural effusion was left sid
ed in three patients and bilateral in five patients. Pleural fluid was char
acterized by lymphocytosis (82 to 99%). Four of the eight patients had a vi
sceral peel and trapped lung requiring decortication. Se, en of the eight b
iopsy specimens showed pleural thickening characterized by dense fibrous ti
ssues with associated mononuclear cell infiltration, while the eighth biops
y specimen showed only clotted blood. The degree of inflammation and fibros
is correlated with the interval between CABG, and pleural surgery. Early po
st-CABG patients displayed more inflammation, with abundant lymphocytes in
nodular configuration deep in the fibrous tissues away from the surface. Ab
undant keratin-positive, spindle-shaped cells were present in the fibrous t
issues. Late cases showed predominantly mature fibrosis.
Conclusions: Persistent post-CABG effusion can occur. Pleural fluids and pl
eural tissue ill early-stage lesions were characterized bq lymphocytosis. W
ith time, the inflammatory changes were replaced by fibrosis that resulted
in dyspnea and, at times, trapped lungs requiring surgical intervention.