WEBINAR REPLAY: "Chest Tube Management in Cardiac Surgery" | ERAS Cardiac Society Webinar in collaboration with CTSNet

Key speakers Marc Gillinov, MD, Jurij M. Kalisnik, MD, and Lenard Conradi, MD discuss the clinical implications of retained blood, current strategies in chest tube management, and the benefits of posterior pericardiotomy.
Webinar moderated by Kevin Lobdell, MD, and Marc Gerdisch, MD.



Leave No Clot Behind: The Role of Clot in Post Operative Fluid Collections

Drainage systems are used to evacuate blood from around the heart and lungs after cardiac surgery. If the drainage capacity exceeds the amount of bleeding, then the blood is fully evacuated. When the drainage capacity is impaired, for example by obstruction from chest tube clots, then blood is retained around the heart (pericardial space) and lungs (pleural spaces). Blood that is retained in these spaces cause a host of complications called retained blood complex (RBC), often impairing patient recovery.

Blood that pools turns to clot. What is the fate of these clots in the pleural and pericardial spaces? It depends on the volume and location. Large volume clots must be surgically evacuated in a re-exploration procedure in the early days after surgery. Smaller, more focal clots that compress the heart can lead to hemodynamic compromise (pericardial tamponade) that can threaten the patient’s life. These can require a subsequent drainage procedure as well.

What about smaller clot collections that are not clinically recognized in the early days after surgery? A number of studies chronicle the reabsorption process of blood in the pleural and pericardial spaces after surgery and suggest that there is an initial breakdown period where the clot contracts and the more solid elements are separated from the fluid elements. This results in a bloody fluid production that is recognizable clinically as pericardial or pleural effusions, and is seen in between 60% and 80% of patients after heart surgery.(1, 2)  When this fluid is examined under the microscope, there are bloody elements as well as inflammatory elements, a finding that correlates with experimental studies that show the pleural or pericardial surfaces remain inflamed throughout the acute, subacute, and chronic phases.(3) This is no surprise as the thrombin contained in the clot is highly pro-inflammatory.(4) This sets up a situation where fluid production, driven in part by vascular endothelial growth factor (VEGF), can continue as the inflammation flares initially, and then simmers before it goes away.(5, 6)

There is a growing appreciation that this may impact the high number of patients who have slow recoveries and even require subsequent fluid drainage procedures and/or readmission after heart surgery. Currently, nearly 14% of cardiac surgery patients are readmitted within 30 days of discharge,(8) and approximately 20% of readmissions are caused by pleural or pericardial effusions.(9)

How can this be minimized? For starters, maximizing early drainage capacity by keeping chest tubes clear has been shown to reduce RBC experimentally, and studies are ongoing to correlate these findings in the clinical setting.(10) Ultimately, becoming more aggressive about “leaving no clot behind” appears to be a strategy that may reduce these complications that impact hospital outcomes and increase long term costs of recovery.


1.         Vargas FS, Cukier A, Hueb W, Teixeira LR, Light RW. Relationship between pleural effusion and pericardial involvement after myocardial revascularization. Chest. 1994;105(6):1748-52.

2.         Light RW, Rogers JT, Moyers JP, Lee YC, Rodriguez RM, Alford WC, Jr., et al. Prevalence and clinical course of pleural effusions at 30 days after coronary artery and cardiac surgery. American Journal of Respiratory and Critical Care Medicine. 2002;166(12 Pt 1):1567-71.

3.         Sadikot RT, Rogers JT, Cheng DS, Moyers P, Rodriguez M, Light RW. Pleural fluid characteristics of patients with symptomatic pleural effusion after coronary artery bypass graft surgery. Archives of Internal Medicine. 2000;160(17):2665-8.

4.         Hott JW, Sparks JA, Godbey SW, Antony VB. Mesothelial cell response to pleural injury: thrombin-induced proliferation and chemotaxis of rat pleural mesothelial cells. American Journal of Respiratory Cell and Molecular Biology. 1992;6(4):421-5.

5.         Marchi E, Broaddus VC. Mechanisms of pleural liquid formation in pleural inflammation. Current opinion in pulmonary medicine. 1997;3(4):305-9.

6.         Grove CS, Lee YC. Vascular endothelial growth factor: the key mediator in pleural effusion formation. Current Opinion in Pulmonary Medicine. 2002;8(4):294-301.

8.         D’Agostino RS, Jacobson J, Clarkson M, Svensson LG, Williamson C, Shahian DM. Readmission After Cardiac Operations: Prevalence, Patterns, and Predisposing Factors. J Thorac and Cardiovasc Surg 1999; 118:823-32

9.         Magnus PC, Chaisson K, Kramer RS, Ross CS, Boss RA, Agha SA, Helm RE, Horton SR, Hofmaster P, Westbrook BM, Duquette D, Quinn RD, Russo L, Jones C, Brown JR, Malenka DJ. Causes of 30-Day Readmission After Cardiac Surgery in Northern New England. Circulation. 2011; 124: A13474

10.       Shiose A, Takaseya T, Fumoto H, Arakawa Y, Horai T, Boyle EM, et al. Improved drainage with active chest tube clearance. Interactive Cardiovascular and Thoracic Surgery. 2010;10(5):685-8.