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The Journal of Thoracic and Cardiovascular Surgery, Vol 105, 823-832, Copyright © 1993 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association
FB Plotz, W van Oeveren, RH Bartlett and CR Wildevuur
Cardiopulmonary bypass for heart operations is associated with a whole body
inflammatory reaction. The main factors involved in this reaction are the
contact system and the complement system. The activation of the contact
system is considered mainly responsible for impaired hemostasis because it
affects platelet function. The activation of the complement system is
considered the main cause for organ dysfunction, particularly of the lung,
due to activation of leukocytes. This study in 10 neonates was undertaken
to evaluate if there are effects of activation of the contact and the
complement systems in neonatal extracorporeal life support comparable to
those during cardiopulmonary bypass for cardiac operations. Two periods of
blood activation during extracorporeal life support could be distinguished.
The initial blood-material interaction at the onset of extracorporeal life
support resulted in activation of both the contact and the complement
systems. The contact activation was apparent by elevated factor XIIa-C1
esterase inhibitor complexes, decreased kallikrein inhibitory capacity,
thrombin-antithrombin III formation, and moderate generation of
fibrin(ogen) degradation products. The complement activation was
characterized by elevated C3a, decreased leukocyte count, elastase release,
and tumor necrosis factor- alpha production. This initial activation
pattern subsided by 24 hours. A second activation period was observed 72
hours after the onset of extracorporeal life support, which was
characterized only by increased clotting and fibrinolytic activity while no
activation of the complement system was observed. We conclude that the
initial activation pattern in extracorporeal life support is similar to
that observed during cardiopulmonary bypass for cardiac operations. The
contact activation that affects platelets might explain the continuous
platelet consumption observed during extracorporeal life support. In this
period, as in cardiopulmonary bypass, aprotinin given in the pump prime
might be effective to prevent platelet consumption and impairment of
hemostasis also in extracorporeal life support. The complement activation
and leukocyte inflammatory reaction during the initial period are able to
cause a capillary leak syndrome and might therefore explain the frequently
observed temporary compromised lung function in extracorporeal life
support. This reaction, as in cardiopulmonary bypass, might be reduced by
the use of specific drugs or heparin coating also in extracorporeal life
support. The cause of the second period of activation during extracorporeal
life support requires further studies before adequate measures can be
recommended.
ARTICLES
Blood activation during neonatal extracorporeal life support
Department of Pediatrics, Neonatology, University Hospital, Groningen, The Netherlands.
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