Adrenal insufficiency in neonates after cardiac surgery with cardiopulmonary bypass.

Background: Cardiopulmonary bypass (CPB) may lead to adrenal insufficiency (AI). Emerging evidence supports association of AI with morbidity after cardiac surgery.

Aims: The aim of this study was to define AI incidence in neonates undergoing complex cardiac surgery with CPB and its association with intraoperative post-CPB outcomes.

Decreasing the Preincision Time for Pulmonary Lobectomy: The Process of Lean and Value Stream Mapping.

Background: Our objective was to evaluate our results after the implementation of lean (the elimination of wasteful parts of a process).

Methods: After meetings with our anesthesiologists, we standardized our "in the operating room-to-skin incision protocols" before pulmonary lobectomy. Patients were divided into consecutive cohorts of 300 lobectomy patients.

Clot lifespan model analysis of the effects of warfarin on thrombus growth and fibrinolysis: role of contact protein and tissue factor initiation.

Warfarin therapy has served as the backbone of chronic anticoagulation therapy for decades to prevent thrombotic morbidity secondary to blood-biomaterial interfaces. Unfortunately, thrombotic and bleeding complications are observed despite maintenance of therapeutic international normalized ratio (INR) values. We proposed to define the effects of warfarin therapy on thrombus growth and disintegration following contact pathway protein or tissue factor (TF) initiation.

Patient with hypofibrinolysis-mediated thromboembolism converted to a hypercoagulable/hyperfibrinolytic state via ventricular assist device placement.

Mechanical circulatory support with ventricular assist devices (VADs) for end-stage heart failure has been a focus of intense interest for nearly four decades. Despite improvements in VAD design and biomaterial composition, it is common to administer anti-coagulation (e.g.

Practical approach to anticoagulation for cardiopulmonary bypass in the patient with congenital prolonged activated partial thromboplastin time.

Patients with rare, congenital deficiencies of contact proteins (e.g., factor XII, prekallikrein, high-molecular-weight kininogen) present an important challenge with regard to safe anticoagulation during cardiopulmonary bypass.

Mechanical circulatory device thrombosis: a new paradigm linking hypercoagulation and hypofibrinolysis.

This review considers the perhaps unappreciated role of contact pathway proteins in the pathogenesis of thrombotic/thromboembolic morbidity associated with mechanical circulatory support. Placement of ventricular assist devices (VADs) has been associated with consumption of circulating contact proteins and persistent generation of activated contact proteins such as Factor XII and high molecular weight kininogen. Importantly, activated contact proteins are absorbed to the surface of VADs via the Vroman effect.

Hemostatic analysis of a 13 year old with antiphospholipid syndrome and restrictive pericarditis.

Antiphospholipid syndrome is an autoimmune thrombophilic disorder that is uncommon in adults and remarkably rare in children. Thrombotic etiological factors are variable in antiphospholipid syndrome, including antibody-antigen complex-mediated platelet activation, inhibition of anticoagulants, or attenuation of fibrinolysis. We present the case of a child with antiphospholipid syndrome presenting with syncope, constrictive pericarditis and hepatic enlargement that was found to have platelet-mediated hypercoagulability and marked clot lysis via thrombelastography in the preoperative period.

The hemostatic history of a 15-month-old child implanted with a Berlin heart left ventricular assist device.

We documented the hemostatic changes associated with placement of a EXCOR Berlin Heart left ventricular assist device in a 15-month-old child before heart transplantation. The development of hypercoagulability was rapid, manifested first by a plasmatic and subsequently platelet-mediated increase in coagulation kinetics and strength that persisted for weeks. The patient had no thrombotic complications for 6 wk before transplant but required extraordinary blood product administration to achieve hemostasis secondary to aggressive, multimodal anticoagulation.

Epsilon-aminocaproic acid inhibition of fibrinolysis in vitro: should the 'therapeutic' concentration be reconsidered?

The therapeutic concentration of epsilon-aminocaproic acid (EACA) has been 130 microg/ml or greater for nearly 50 years. We tested the effects on clot growth/disintegration of EACA with a plasmatic model of hyperfibrinolysis in vitro. Human plasma was exposed to 1000 U/ml tissue-type plasminogen activator containing 0, 13, 65 or 130 microg/ml EACA, with clot growth/disintegration kinetics quantified via thrombelastography.

Qualitative thrombelastographic detection of tissue factor in human plasma.

Background: Tissue factor (TF) is the principal in vivo initiator of coagulation, with normal circulating TF concentrations reported to be approximately 23-158 pg/mL. However, patients with atherosclerosis or cancer have been reported to have TF concentrations ranging between 800 and 9000 pg/mL. Of interest, thrombelastographic (TEG)-based measures of clot initiation and propagation have demonstrated hypercoagulability in such patients at risk for thromboembolic events.

Contact activation prolongs clot lysis time in human plasma: role of thrombin-activatable fibrinolysis inhibitor and Factor XIII.

Background: Contact activation system proteins (e.g., Factor XII, kallikrein) have been implicated as direct or indirect activators of plasminogen.

Argatroban, bivalirudin, and lepirudin do not decrease clot propagation and strength as effectively as heparin-activated antithrombin in vitro.

Background: Heparin-induced thrombocytopenia is a potentially limb- and life-threatening response to heparin exposure. Direct thrombin inhibitors (DTIs) have been reported to provide anti-coagulation for cardiopulmonary bypass; however, clot formation within the cardiopulmonary bypass circuit has been reported after the administration of DTIs. We present a case of thrombosis of the cardiopulmonary bypass circuit and, ultimately, death after argatroban administration.