Bleeding begets Bleeding

CardioThoracic surgeons have all seen take-backs for "bleeding" and found no "bleeder". A washout suffices to end the vicious cycle of oozing and clotting that can go on for days.

Why?

RETAINED BLOOD.

Why?

Because the regular chest tubes you use today block 100% of the time. 36% of the time they are completely occluded. 86% of the time that occlusion is under the skin line and invisible as well as deceiving. (Karimov, Eur J Cardiothorac Surg. 2013, â€œIncidence of chest tube clogging after cardiac surgery: a single-centre prospective observational study”)

Retained Blood quickly initiates an aggressive inflammatory and auto-immune response that can trigger POAF and will always generate effusions. Hemolysis gets underway, reactive oxygen species harmfully proliferate from hemoglobin metabolites (what Kramer, Melby et al called hemoglobin oxidative induced stress https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4422823/) and white cell recruitment ramps up that release hydrogen peroxide on-site. Massive hemolytic, fibrinolytic and thrombinolytic efforts result with elevated VGEF and tPA markers. And the oozing will go on and on as water accumulates and your also blood-blocked Blake drain begins to weep effusions as capillary pressure builds. But you have failed to get the blood out in the first 12 hours. The Blake drains narrow but high surface area canals of thrombogenic plastic was blocked with clot in the first two hours. Your regular mediastinal drain was blocked. And bleeding begets bleeding.

There is a better way. PleuraFlow is the only FDA cleared device indicated to prevent Retained Blood. 50,000 cases on and we are the world leader in post-op blood evacuation now. www.clearflow.com

Negative Reexploration for Cardiac Postoperative Bleeding: Can It Be Therapeutic?

Marc P. Pelletier, MD, Susan Solymoss, MD, Andrew Lee, BSc, and Ray C.-J. Chiu, MD, PhD

Divisions of Cardiothoracic Surgery and Hematology, The Montreal General Hospital, McGill University, Montreal, Quebec, Canada

Background. Reexploration of the mediastinum for bleeding is required in 3% to 7% of patients after cardiac operation, with many proving to have no surgically correctable cause. In spite of a “negative exploration,” the bleeding often ceases. We propose the hypothesis that such a negative exploration can be therapeutic by reduc- ing marked fibrinolytic activity in the mediastinal cavity.

Methods. Fibrinolytic activity in shed mediastinal blood was compared with that in the system blood in 5 patients after cardiac operation by measuring fibrinogen, fibrin degradation product, plasminogen activator inhib- itor-1, and ??2-antiplasmin levels.

Results. Fibrinolytic activity in mediastinal blood was markedly increased when compared with paired sys- temic venous blood. This was indicated by the medias- tinal blood’s lower fibrinogen levels (0.47 versus 1.91 U/mL; p < 0.001), very high levels of fibrin degradation products (1,350 versus 200 ng/mL; p < 0.05), and higher levels of plasminogen activator inhibitor-1 (55.5 versus 28.1 ng/mL; p < 0.005). Decreased levels of ??2-antiplas- min were also observed in the mediastinum (0.50 versus 0.61 U/mL; p < 0.05).

Conclusions. Our data confirm that fibrinolytic activity can be extremely high in the mediastinum in response to clot formation. This may explain the hemostatic effects of a negative reexploration, where irrigation and the re- moval of clots may reduce the fibrinolytic process; this may allow the bleeding ends of capillaries and small vessels to thrombose. Decreased levels of ??2-antiplasmin observed suggest that lysine analogs, such as ??-aminoca- proic acid, may have a beneficial role when locally delivered into the mediastinum.

(Ann Thorac Surg 1998;65:999–1002)