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Ann Thorac Surg 2006;81:S2360-S2366
© 2006 The Society of Thoracic Surgeons

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Supplement

Coagulopathy and Inflammation in Neonatal Heart Surgery: Mechanisms and Strategies

^a Department of Pediatric Cardiothoracic Surgery, Duke University Medical Center, Durham, North Carolina
^b Division of Vascular Surgery, Department of Surgery, Duke University Medical Center, Durham, North Carolina

^_* Address correspondence to Dr Jaggers, Department of Pediatric Cardiothoracic Surgery, Duke University Medical Center, Durham, NC 27710. (Email: Jagge003@mc.duke.edu).

Presented at the Symposium on Harnessing the Effects of Neonatal Cardiopulmonary Bypass at the Fourth World Congress of Pediatric Cardiology and Cardiac Surgery, Buenos Aires, Argentina, Sept 21, 2005.

The first 300 words of the full text of this article appear below.

	Introduction

 
Open cardiac surgery has enjoyed significant improvement in outcome during the last several years. Complex heart defects once considered fatal are now readily addressed with low mortality. However, repair of these defects requires the use of cardiopulmonary bypass (CPB), which results in significant alteration of normal homeostatic mechanisms. Normal hemostasis reflects a highly complex interaction between endothelial cells, platelets, local and systemic inflammatory mediators, and coagulation factors [1, 2]. The inflammatory and coagulopathic complications are manifest as diffuse capillary leak syndrome, coagulopathy, respiratory failure, myocardial dysfunction, renal insufficiency, and neurocognitive defects [3]. Clinical experience reinforces that these adverse effects seem to be more pronounced in neonates and young infants as compared with older children. In this review we will discuss the pathophysiology of coagulation in neonates and small infants undergoing open cardiac surgical repairs and discuss existing and potentially strategies directed toward limiting coagulopathy.

	Normal Hemostasis in Neonates and Infants

 
At birth, concentrations of the vitamin K–dependent clotting factors (FII, FVII, FIX, and FX) and contact factors (FXI and FXII) are reduced to about 50% of normal adult levels, and natural anticoagulant and inhibitory factors (antithrombin III, protein C, protein S, CI esterase inhibitor, and plasminogen) are similarly reduced [4]. This may be a result of decreased hepatic synthesis and accelerated clearance caused by increased metabolic rates [5]. There may also be a functional immaturity of the normal mechanisms of coagulation factor binding in neonates. In adults, coagulation remains intact with factor levels as low as 30% for all factors except factor V, which requires only 15% of normal levels for normal function [6]. In neonates functional integrity of the coagulation system is also preserved in the presence of decreased factor levels as measured by thromboelastography [7]. Because healthy term and premature infants do . . . [Full Text of this Article]

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