PubMed · 14101821
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
B BERKARDA, U DERMAN. 1963. [HYPERCOAGULABILITY AND A NEW HEPARIN LOADING TEST].. https://pubmed.ncbi.nlm.nih.gov/14101821/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Explore the source record for details and available documents.
Platelet aggregation at sites of vascular injury is essential for the formation of the primary haemostatic plug. The mechanism of platelet aggregation under conditions of physiological flow is a complex multistep process, which requires the synergistic action of several different platelet receptors. Platelet interaction with collagen at sites of damage to the vascular endothelium involves adhesion, activation, secretion of platelet granular contents and finally aggregation. Other agonists other than collagen, such as fibrinogen, vWF and soluble agonists released from activated platelets (thromboxane A2 (TXA2) and ADP) are involved in platelet aggregation. Platelets express a variety of receptors including GP Ib-IX-V, GP VI, GP Ia-IIa and GP IIb-IIIa. One aspect of this complexity of function is the variety of inherited defects of platelet function. Hereditary disorders of platelet adhesion are Bernard-Soulier syndrome and von Willebrand disease. Glanzmann thrombasthenia is an inherited disorder of platelet aggregation. The application of molecular biology to the study of platelet disorders has identified defects in other collagen receptors, ADP receptors and TXA2 receptors. Defects affecting TXA2 production, the generation of procoagulant activity and secretion from dense bodies and alpha-granules are also encountered. Other rare diseases, Chediak-Higashi, Hermansky-Pudlak and Wiskott-Aldrich syndrome also affect platelet storage granules. In this article, recent advances in the understanding of platelet function and knowledge of inherited disorders that affect platelet adhesion and aggregation is reviewed. As progress advances towards individualisation of therapy the phenotypic bleeding tendency of each patient becomes relevant.
Liver surgery has long been associated with massive perioperative blood loss and high rates of postsurgery morbidity and mortality. Recent advances in our knowledge of hepatic segmental anatomy have led to the evolution of liver resection, and a growing awareness of the coagulopathy present in cirrhotic patients has produced a greater understanding of the factors influencing surgical hemostasis. This review will examine the risk factors for perioperative hemorrhage in liver disease patients, and will describe current pharmacological, surgical, and radiological methods available for controlling bleeding and achieving effective hemostasis during liver resection and orthotopic liver transplantation (OLT). The potential role of recombinant factor VIIa (rFVIIa) in providing safe hemostasis during such procedures will also be explored. Today, due to careful monitoring and correction of coagulopathy, improved surgical techniques, and judicious patient selection, liver surgery is no longer a high-risk specialty with an unfavorable risk profile, but a safe and widely practiced procedure.