Ann Thorac Surg 1999;68:1062-1063
© 1999 The Society of Thoracic Surgeons
Case Reports
A minimally invasive approach to chylopericardium after coronary artery surgery
David A.C. Sharpe, FRCSa,
Mark D.M. Pullen, FRCSa,
Joseph P. McGoldrick, FRCSa
a Department of Cardiothoracic Surgery, The Yorkshire Heart Centre, The General Infirmary at Leeds, Leeds, United Kingdom
Address reprint requests to Dr Sharpe, Department of Cardiothoracic Surgery, The General Infirmary at Leeds, Great George St, Leeds, LS1 3EX, United Kingdom
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Abstract
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We report a case of chylopericardium and chylothorax after coronary artery bypass grafting, which presented as delayed cardiac tamponade. We describe the minimally invasive management of a condition that can be associated with a protracted surgical course.
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Introduction
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Chylopericardium remains a rare entity, usually associated with complex procedures requiring extensive surgical dissection within the pericardium [1, 2]. Four cases of chylopericardium have been reported after coronary artery bypass grafting (CABG), though none in association with chylothorax [36]. We present a case of combined chylothorax and chylopericardium and discuss management strategies for a perplexing clinical condition.
A 63-year-old woman with triple-vessel coronary artery disease underwent routine CABG with four saphenous veins. At surgery, the internal thoracic artery was not harvested, the pleurae were intact, and the thymus was not excised. Cardiopulmonary bypass was established using a single two-stage venous cannula, without caval snares, and arterial return was to the ascending aorta. There was minimal dissection of the aorta, sufficient only to apply an aortic cross-clamp. No tape was passed around the aorta, and there was no dissection around the pulmonary artery. Anesthetic venous access was achieved with a single right-sided internal jugular venous catheter.
She had an uneventful operative course, made a good recovery, and was discharged home fit and well on the 7th postoperative day. A chest radiograph on the day before discharge showed no signs of cardiomegaly or cardiac failure.
She represented to the cardiothoracic unit as an emergency on the 11th postoperative day showing signs of cardiac tamponade. A chest radiograph demonstrated gross cardiomegaly and a left-sided pleural effusion. Initial management was subxiphisternal pericardial drainage under ultrasound guidance using a "pigtail" catheter. Drainage of 300 mL of turbid fluid brought immediate hemodynamic improvement. Laboratory examination of the fluid showed it to be sterile chyle. She continued on a normal diet and drained intermittently from the pericardial catheter between 400 and 850 mL of chyle daily for the next 5 days. Curiously, during this period, the left-sided effusion increased in size (Fig 1).

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Fig 1. Plain chest radiograph demonstrating gross cardiomegaly and left-sided pleural effusion as the patient represented on the 11th postoperative day with signs and symptoms of cardiac tamponade.
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In view of the persisting drainage, the management was revised, the "pigtail" pericardial drain was removed under general anesthesia, and replaced with a larger drain (28 French gauge) (Portex; Simms Medical Distribution, Hythe, Kent, UK); a left-sided pleural drain (28 French gauge) (Portex) was also inserted. A tunneled feeding line was introduced into the left subclavian vein. Finally, a pericardial washout with a weak Betadine (Seton Healthcare Group PLC, Oldham, Lancashire, UK) solution (0.5% Betadine in normal saline) performed. The left-sided pleural effusion was found to be sterile chyle.
Postoperatively, she was kept "nil by mouth" and parentral nutrition was instituted; drainage from the pericardial tube diminished rapidly in the first 3 days of this management regime. By the 9th day of parenteral nutrition, chylous drainage had completely stopped. Diet was reinstituted with no recurrence of drainage; all drains were removed 48 hours after diet recommenced. Repeat ultrasound examinations and chest radiographs where performed before discharge, 18 days after readmission, with no evidence of reaccumulation of pericardial or pleural fluid.
Subsequent review at out patient clinic 18 months postoperatively found her to be well, with no recurrence of chest pain, or symptoms suggestive of pericardial disease. Chest radiography and ultrasound examinations confirmed no further reaccumulation of pericardial or pleural effusions.
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Comment
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The etiology of chylopericardium after cardiac surgery is thought to involve disruption of the cardiac lymphatic channels in the pericardial reflections during surgery. In this reported case, minimal dissection was enough to precipitate a large and life-threatening chylopericardium. It is apparent that any dissection within the pericardium can potentially cause this problem. Pollard and Bakay, who both reported chylopericardium after CABG, implicated venous thrombosis as a causative factor, and other authors have suggested this as a mechanism after other cardiac surgical procedures [1, 3, 5]. Pollard and associates suggest that occlusion of the thorax duct drainage by thrombosis leads to a rise of pressure within the lymphatic system, and back-flow from this through ruptured lymphatic vessels is the pathophysiological basis of postoperative chylothorax [3]. Our own case shows no evidence of venous thrombosis, and therefore would not support the view that this is the mechanism in the pathogenesis of chylopericardium.
A variety of management regimens have been employed in the treatment of chylopericardium. Patients who present with cardiac tamponade often have open surgical drainage of the pericardial fluid, and in some cases, a subsequent drainage procedure for the resulting chylothorax [3, 4]. We found that the simple introduction of a "pigtail" catheter under ultrasound guidance was sufficient in the short term to control this condition. Our conservative and expectant approach of pericardial and pleural drainage combined with parentral nutrition contrasts sharply with the surgical intervention. Surgical drainage of the pericardium does not tackle the fundamental problem of disrupted lymphatic channels [3].
We conclude that delayed chylous pericardial effusions can be a life-threatening complication after cardiac surgery, it can occur after even the minimal dissection in the pericardium associated with CABG in the absence of other exacerbating factors. We would commend the practice of minimal intervention as a safe and logical course of management for this perplexing condition.
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References
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Accepted for publication January 22, 1999.
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