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Symptomatic Persistent Post-Coronary Artery Bypass Graft Pleural Effusions Requiring Operative Treatment^*

Clinical and Histologic Features

^* From the Departments of Pulmonary Medicine (Dr. Lee) and Pathology (Dr. McDonald) and Cardiovascular Surgical Associates (Dr. Nesbitt), Saint Thomas Hospital, Nashville, TN; the Pulmonary Division (Dr. Vaz), Heart Institute (INCOR), University of Sao Paulo Medical School, Sao Paulo, Brazil; the Departments of Pathology (Dr. Ely) and Medicine (Dr. Light), Vanderbilt University, Nashville, TN; and the Department of Medicine (Dr. Thompson), University of Western Australia,

Correspondence to: Y. C. Gary Lee, MBChB, Department of Pulmonary Medicine, Saint Thomas Hospital, 4220 Harding Rd, Nashville, TN 37202; e-mail: ycgarylee{at}hotmail.com

Background: More than 85% of patients develop pleural effusions after coronary artery bypass grafting (CABG). Although the majority resolve spontaneously, post-CABG effusions can persist. The cause of these persistent effusions is unknown, and the histology of the pleural changes has seldom been reported.

Objectives: To describe the patient characteristics and pathologic condition 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. These eight patients were selected as having undergone CABG > 2 months before 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% (range, 15 to 70%). All patients were dyspneic and had large ( 25% of the hemithorax) effusions on chest radiograph. All effusions persisted after two or more thoracenteses. Pleural effusion was left sided in three patients and bilateral in five patients. Pleural fluid was characterized by lymphocytosis (82 to 99%). Four of the eight patients had a visceral peel and trapped lung requiring decortication. Seven of the eight biopsy specimens showed pleural thickening characterized by dense fibrous tissues with associated mononuclear cell infiltration, while the eighth biopsy specimen showed only clotted blood. The degree of inflammation and fibrosis correlated with the interval between CABG and pleural surgery. Early post-CABG patients displayed more inflammation, with abundant lymphocytes in nodular configuration deep in the fibrous tissues away from the surface. Abundant keratin-positive, spindle-shaped cells were present in the fibrous tissues. Late cases showed predominantly mature fibrosis.

Conclusions: Persistent post-CABG effusion can occur. Pleural fluids and pleural tissue in early-stage lesions were characterized by lymphocytosis. With time, the inflammatory changes were replaced by fibrosis that resulted in dyspnea and, at times, trapped lungs requiring surgical intervention.

Key Words: coronary artery bypass grafting • pathology • pleural effusion

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