The diagnosis and monitoring of hematological malignancies is complex and requires a systematic approach. Morphology, cell phenotyping, cytogenetics and molecular genetics are essential, and the results must be integrated. Diagnostic Techniques in Hematological Malignancies details the principles and applications of each of these test types in the diagnosis of hematological malignancies in blood and bone marrow. The first section describes the test modalities - including methodological principles, data interpretation and limitations - and is illustrated by clinical examples. The second section focuses on the clinical entities, detailing the most appropriate tests for diagnosis, staging and monitoring of different hematological malignancies and includes test utilization to identify prognostic markers and potential therapeutic targets. With contributions from multiple international experts, this illustrated book is an essential resource for qualified and trainee hematologists, oncologists, and pathologists. It's a practical and useful guide, providing a rational and structured approach to the laboratory assessment of hematological malignancies.

The authors summarise advances in human pluripotent stem cells-derived erythroid development and molecular regulatory mechanisms. This research may provide a new perspective on human embryo erythropoiesis and a possible treatment for some hematological diseases. Erythrocytes are well equipped to carry out their functions due to a dynamic cell membrane, their inherent shape and lack of organelles and cytoplasmic viscosity. As such, the following section focusses on the causes of these modifications and their clinical implications. As an example of complexity in research towards the development of erythrocyte membrane-based drug delivery systems starting from animal erythrocyte, morphological, biochemical and drug release profiles will be reviewed in the penultimate chapter. The final chapter investigates the electrochemical behavior of erythrocytes at platinum, carbonaceous, and optically transparent electrodes via polarization and coulometric measurements. The order of magnitude of the quantity of electrons transferred between erythrocytes and electrodes was determined, and potential ranges showing indifference of the electrode toward red blood cells were identified.

Text in French.

Prevailing physiological concepts (PPC) of blood circulation consider the cardiovascular system (CVS) an autonomous system that has its own goal and mechanisms for achieving it. Physiologists agreed that complex neural and humoral controllers of a mean arterial pressure (MAP) indirectly alter the blood flows for satisfying cellular needs. However, PPCs are incapable of explaining the causes of long-term shifts of an MAPs rest level. In particular, this affects current understanding and cure technologies of arterial hypertension (AH). Considering AH as a disease, physicians seek a cure that effectively decreases the elevated pressure. This gave rise to the palliative cure softening of AH symptoms without an understanding of AHs primary causes. But this strategy, working until the patient intakes antihypertensive drugs, often leads to AHs further development, and in extreme cases current antihypertensive drugs are helpless. These limitations of PPC are forced to seek a circulations extended physiological theory (EPT), explaining the mechanisms of both normal and altered MAPs. In the EPT presented in the book, CVS is considered a constituent part of a more complex functional super-system (FSS) that appeared in a multi-cellular animal organism during the co-evolution of specialized cells. The general goal of the FSS is to provide optimal physiochemical and energy states of the cell cytoplasm. To achieve this goal under a stochastic total and local variations of cells activity, FSS should control: i) The cardiac output; ii) the regional and local blood flows; and iii) the chemical composition of both arterial and venous blood. Under chronic energy shortage, FSS should also provide an adequate increasing of ATP-synthesis in mitochondria of stagnated cells. So, under the ineffectiveness of current mitochondria, FSS must enrich the arterial blood by chemicals providing the biogenesis of mitochondria. However, neither the energy providers nor the providers of blood chemistry are properly involved in PC of the blood circulation. The EPT for the first time integrates the hemodynamic and metabolic aspects of cell life at the organism scale. It is proved that the CVS activity is inversely associated with the activity mechanisms controlling the rates of both pulmonary ventilation and erythropoiesis. Under significant and chronic energy deficiency, the cells activate additional FSS mechanisms, materially supporting the biogenesis of mitochondria. The activity of FSS mechanisms forming the chemical composition of arterial and venous blood is in reciprocal relationships with the function of CVS. So, the EPT associates the function of CVS with energy and metabolic problems in cells. The EPT concerns both traditional and additional determinants of the MAP level. It is proved that stochastic combinations of these determinants force the MAP level to float. In particular, both the mitochondrial insufficiency and the chemical contamination of cytoplasm are capable of causing AH. The normal arterial pressure is always individual. Before correcting the altered arterial pressure, a complex medical examination for ascertaining the mitochondrial function, the status of the FSS mechanisms is recommended. The diagnosis of AH should be reoriented for detecting cellular abnormalities. The therapy of AH should be targeted at finding strategies for the optimizing the entire FSS function.

Cyclic AMP was a major molecule of interest, which played an important role as second messenger, contributing to signal transduction in the regulation of cellular function by peptide hormones. Afterwards, calmodulin and protein kinase C were discovered as modulator proteins of intracellular calcium signaling in hormonal action. After that, manifold proteins and their related molecules were demonstrated to participate in novel signaling pathways related to various cytokines in different types of cells. The author of this book discovered a novel protein known as regucalcin, which suppresses manifold signaling pathways related to transcription activity. After subsequent studies, regucalcin has been established to play a pivotal role in maintaining cell homeostasis and protecting it from disorders in various types of cells and tissues. This book will provide information regarding regucalcin that plays a pivotal role in cell homeostasis and disorder. This book is composed of eighteen chapters. These chapters include the following content: the discovery of regucalcin (Chapter One); chemical property and structure of regucalcin (Chapter Two); the regucalcin gene and its translational regulation (Chapter Three); the role of regucalcin in intracellular calcium homeostasis (Chapter Four); the role of regucalcin in cell nuclear function (Chapter Five); the role of regucalcin in protein synthesis and proteolysis (Chapter Six); the suppressive role of regucalcin in cell proliferation (Chapter Seven); how regucalcin protects apoptotic cell death (Chapter Eight); the protective role of regucalcin in oxidative stress (Chapter Nine); the involvement of regucalcin in liver metabolic disorder (Chapter Ten); the role of regucalcin in kidney cell homeostasis: involvement in renal failure (Chapter Eleven); the role of regucalcin in heart calcium signaling: insight into cardiac disorder (Chapter Twelve); the role of regucalcin in brain calcium homeostasis: disorder with aging (Chapter Thirteen); the role of regucalcin in bone homeostasis and osteoporosis (Chapter Fourteen); the role of regucalcin in lipid metabolism and diabetes (Chapter Fifteen); the role of regucalcin as a suppressor protein in carcinogenesis (Chapter Sixteen); the clinical aspects of regucalcin as a biomarker for disease (Chapter Seventeen); and conclusive remarks (Chapter Eighteen). This book will provide information regarding regucalcin and its pivotal role in cell homeostasis and disorder.

Sickle cell disease (SCD), an inherited hemolytic anemia, is associated with multiple acute and chronic complications such as painful vasoocclusive events, cerebral vasculopathy, priapism, and renal or lung disease. These complications are variable and unpredictable, and can be associated with significant morbidity and poor quality of life. This book covers several areas regarding pathology, diagnosis, complications, signs, symptoms and medical treatments. There are few studies in literature on the role of physiotherapy as a resource to prevent and treat locomotor system disorders, respiratory problems and painful crises in SCD individuals. This book highlights the role of physiotherapy in sickle cell anemia. A comprehensive and authoritative monograph, this book will be equally interesting to both established researchers and to graduate students interested in both genetics and the physical therapy field.

Acute myeloid leukemia (AML) is an aggressive bone marrow cancer associated with high morbidity and mortality and most commonly affects older patient populations. In this book, the clinical presentation of acute myeloid leukemia are presented. Other chapters present the differences in the outcomes of two subtypes of core binding factor (CBF) acute myeloid leukemia (AML); examine the occurrence of the Philadelphia chromosome in AML with core binding factor leukemia; and therapeutic options of older patients with AML.

Sickle cell hemoglobin (HbS) is the result of a single nucleotide change (GAG GTG) in the beta-globin gene, where valine replaces glutamic acid at the sixth amino acid position in the beta-globin chain. Sickle cell disease is a growing global health problem. The World Health Organization has estimated that 7% of the world population has the mutation and 300,000400,000 affected children are born every year. The disease progresses towards a severe chronic hemolytic anemia, and it shows a heterogeneous clinical course, related with different genetic factors. Despite the fact that all subjects with sickle cell disease (SCD) have the same single base pair mutation in the DNA, we further confirmed here that the severity of the clinical and hematological manifestations is extremely variable. Increasing evidence has indicated a role of oxidative stress in the vascular pathophysiology of SCD. The vascular endothelium is central to disease pathogenesis because it displays adhesion molecules for blood cells, balances procoagulant and anticoagulant properties of the vessel wall and regulates vascular homeostasis by synthesizing vasoconstricting and vasodilating substances.In addition, recent studies support the existence of a hyperoxidative status in SCD patients that may account, at least in part, for the clinical manifestations of these patients. Moreover, SCD patients with mild clinical outcomes were associated with low oxidative status, whereas high oxidative stress was related to severe phenotypes. Thus, the use of oxidative stress biomarkers may be important in the evaluation of the clinical condition of SCD patients, whereas the use of therapies to improve their redox status and increase NO bioavailability would be beneficial to reduce the severity of sickle disease. The global burden of SCD is now significantly increased and, thus, it is currently a public health problem around the world. This disease has passed from being a problem of the developing countries to affect many people in developed countries. This book summarizes the current epidemiology status and the latest discoveries in the pathophysiology of SCD, and the potential therapies that may improve the clinical course of this disease.

Neutrophil granulocytes are the primary defense cells of blood against bacteria, fungi, parasites, or thrombi. Their main weapons and signals are reactive oxygen species (ROS) that release photons. The activation of the assembly of their NADPH-oxidase, the few specific triggers and many specific or unspecific primers are of great physiological and pathophysiological importance in inflammation and in hemostasis. The neutrophils generate different types of photons and they can "see" them. The 300400 nm photons are the main signals and the photons of lowest wave length which seem to especially alert them in emergency. The present book presents research on the regulation of the neutrophil's ROS generation by different photons, by singlet oxygen (the excited "pro-drug" of photons), by important proteins, or by modulators of the eicosanoid metabolism that should not favor the generation of systemically circulating micro-thrombi.

Transfusion Medicine is a key part of modern health care. It bridges the healthy community with the bedside in hospitals. It is the responsibility of the national blood program to provide an adequate supply of blood for all patients requiring transfusion, and to ensure the quality of blood and blood products for clinical use and the in-hospital transfusion chain. All products must be safe, clinically effective and of appropriate, and consistent quality. Every blood transfusion service, whether serving in a resource restricted environment or in an advanced ambience, should develop an effective quality (QS) and quality management system (QMS) to ensure the implementation of these strategies from vein to vein. The quality system and its management should cover all aspects of its activities and ensure full traceability (hemovigilance), from the motivation, mobilisation and selection of blood donors to the transfusion of blood and blood products to patients. It should also reflect the structure, needs and capabilities of the procurement establishments, as well as the needs of the hospitals and patients that it serves. Management commitment and support are essential for the development, implementation and monitoring of a national quality system and quality management system in order to ensure change management and continuous quality improvement. All staff should understand the importance of quality and the consequences of failure in the quality system (error management and cost effectiveness).

Hemostasis (coagulation and fibrinolysis) is of importance in a broad range of medical disciplines. A high-quality hemostasis diagnosis enables a good therapy, which can be rather complicated without laboratory help. This yearbook gathers important contributions in this field and presents them in a coherent and logical format.

For many years the mammalian blood cell system has provided cell biologists and haematologists with one of the best experimental models in which to unravel how one stem cell -- the hematopoietic stem cell -- gives rise to many different types of progeny. Numerous models of lineage relationships have emerged, but the most influential of these, in which differentiating cells undergo a series of binary choices, has been increasingly challenged in recent years -- to the extent that the accumulation of new findings recently culminated in a Nature commentary suggesting that "the latest research will necessitate revision of textbook accounts". This book brings together contributions from many leading experts in the field of blood cell development who each discuss both the overall process of hematopoiesis and the origins and development of each of the cells of the blood and immune systems. It describes how new molecular, cellular and -- particularly -- transgenic tools are helping us understand the processes that control the lineage fates of hematopoietic stem and progenitor cells and how lineage-committed progeny develop along particular maturation pathways.

Granulocytes are a category of white blood cells characterised by the presence of granules in their cytoplasm. This book examines the characteristics of eosinophil granulocytes, its biological functions, its role in inflammation and its clinical significance in children. This book also reviews the role of granulocytes on the onset of tissue-destructive diseases when exposed to stress. In addition to the cases of disease, some physiological phenomena are also responsible for the stress-induced granulocytosis. Thus this book will also expands upon the role of granulocytes associated with various diseases and some physiological responses. Other topics discussed in this book include the role of basophil, the minute group of granulocyte, in tropical infections and in immune regulations; polymorphonuclear neutrophilic granulocytes (neutrophils), which are the most dangerous cells in the organism and their role in transient states of autoimmunity, and the effects of nucleoli change during differentiation and maturation of granulocytes.

Hematopoietic stem cell transplantation (HSCT) is the transplantation of blood stem cells derived from the bone marrow (that is, bone marrow transplantation) or blood. Stem cell transplantation is a medical procedure in the fields of haematology and oncology, most often performed for people with diseases of the blood, bone marrow, or certain types of cancer. Stem cell transplantation was pioneered using bone-marrow-derived stem cells by a team at the Fred Hutchinson Cancer Research Center from the 1950s through the 1970s led by E. Donnall Thomas, whose work was later recognised with a Nobel Prize in Physiology and Medicine. Thomas' work showed that bone marrow cells infused intravenously could repopulate the bone marrow and produce new blood cells. His work also reduced the likelihood of developing a life-threatening complication called Graft-versus-host disease. With the availability of the stem cell growth factors GM-CSF and G-CSF, most hematopoeitic stem cell transplantation procedures are now performed using stem cells collected from the peripheral blood, rather than from the bone marrow. Collecting stem cells provides a bigger graft, and does not require that the donor be subjected to general anaesthesia to collect the graft. Hematopoeitic stem cell transplantation remains a risky procedure with many possible complications; it has always been reserved for patients with life-threatening diseases. This book presents recent leading research in the field.

Warfarin (also known under the brand names of Coumadin, Jantoven, Marevan, and Waran) is an anticoagulant medication that is administered orally or, very rarely, by injection. It is used for the prophylaxis of thrombosis and embolism in many disorders. Its activity has to be monitored by frequent blood testing for the international normalised ratio (INR). It is named for the Wisconsin Alumni Research Foundation. Warfarin is a synthetic derivative of coumarin, a chemical found naturally in many plants, notably woodruff (Galium odoratum, Rubiaceae), and at lower levels in liquorice, lavender and various other species. Warfarin was originally developed as a rat poison; however, more modern poisons are much more potent and toxic (e.g., brodifacoum). Warfarin and contemporary rodenticides belong to the same class of drugs (coumarins) and both decrease blood coagulation by interfering with vitamin K metabolism. For this reason, drugs in this class are also referred to as vitamin K antagonists.

There are two dominant aspects which conclude the coagulation cascade: the importance of the tissue factor pathway in initiating clotting and the interaction between pathways. Two main pathways are recognised the extrinsic and the intrinsic. At the side of vascular injury endothelial cells are converted in a pro-thrombotic state or become detached to exposed circulating blood to thrombogenic constituents of the sub-endothelial matrix. Activation of platelets and formation of fibrin occur simultaneously and interdependently to effect haemostasis. The activated platelets express the receptor GPIb-IX-V complex that further strengthens the adhesion by linking to von Willebrand factor expressed on the sub-endothelial matrix. A platelet monolayer which covers the injured area recruits and aggregates activated platelets to form a platelet plug by linking to fibrinogen molecules. Activation of a series of inactive precursors leads to the formation of thrombin that cleaves fibrinogen to fibrin. The sequence of reactions interacting between factor X represents the common pathway of coagulation. Factor X can be activated in turn by either the tissue factor pathway or the contact activation pathway of coagulation, which is initiated by the complex of tissue factor and factor VIIa. The latter involves a series of zymogen protease reactions that are initiated by contact activation of factor XII to XIIa. As the haemostatic process starts, a series of inhibitory mechanisms is activated involving antithrombin III, protein C, protein S, the tissue factor pathway inhibitors 1 and 2 and platelet inhibitors (prostaglandin I2, nitric oxide). Fibrinolytic mechanisms assure the clot's remodelling and elimination in the prospect of restoring the vessels patency. During the fibrinolytic process plasmin cleaves polymerised fibrin to fibrin degradation products. The liver plays a predominant role in the regulation of haemostasis. By producing most clotting factors (except tissue factor TF) and inhibitors (antithrombin III, protein C, protein S, C1 inhibitor), as well as a number of the proteins involved in fibrinolysis (plasminogen, a2-antiplasmin), and by clearing from the bloodstream activated enzymes involved in clotting or fibrinolysis, the liver protects against both bleeding and overwhelming activation of coagulation. There is a common bleeding profile emerging in the overwhelming majority of liver diseases. The severity of documented coagulation disorders varies analogically to the degree of the hepatocellular injury. The importance of the coagulopathy is underlined by the incorporation of the coagulation parameters into prognostic scores assessing fulminant hepatic failure and cirrhosis. The purpose of this book is to review the coagulation profile in acute liver failure, liver cirrhosis, autoimmune cholestatic, viral and various hepatic diseases. Diagnostic and therapeutic modalities in coagulation defects in liver diseases are also reviewed.

The proposed book focuses on 'blood infections', a common group of haematology and infectious disorders in aspects relating to the tropical medicine. The book covers specifically the clinical aspects, scientific laboratory aspects, public health aspects, as well as the social sciences relating to these important diseases. The common blood infections, including other disorders, which relate to blood disorders are summarised, presented, and discussed. The book presents summative data from the molecular to the population scales, as well as additional metanalysis for important topics.

Sickle cell anaemia is an inherited blood disorder, characterised primarily by chronic anaemia and periodic episodes of pain and occurring in approximately 1 in every 400 African-American infants born in the United States each year. Individuals of Mediterranean, Arabian, Caribbean, South and Central American, and East Indian ancestry can also be affected. The underlying problem involves haemoglobin, a component of the red cells in the blood. The haemoglobin molecules in each red blood cell carry oxygen from the lungs to the body organs and tissues and bring back carbon dioxide to the lungs. In sickle cell anaemia, the haemoglobin is defective. After the haemoglobin molecules give up their oxygen, some of them may cluster together and form long, rod-like structures. These structures cause the red blood cells to become stiff and to assume a sickle shape. Unlike normal red cells, which are usually smooth and donut-shaped, the sickled red cells cannot squeeze through small blood vessels. Instead, they stack up and cause blockages that deprive the organs and tissue of oxygen-carrying blood. This process produces the periodic episodes of pain and ultimately can damage the tissues and vital organs and lead to other serious medical problems. Unlike normal red blood cells, which last about 120 days in the bloodstream, sickled red cells die after only about 10 to 20 days. Because they cannot be replaced fast enough, the blood is chronically short of red blood cells, a condition called anaemia. Sickle cell anaemia is caused by an error in the gene that tells the body how to make haemoglobin. The defective gene tells the body to make the abnormal haemoglobin that results in deformed red blood cells. This book gathers the latest research in this important field.

Angiogenesis -- the growth of new blood vessels -- is an important natural process occurring in the body, both for health and as related to disease. Angiogenesis occurs in the healthy body to help heal wounds and to help restore blood flow to tissues after injury or insult. In females, Angiogenesis also occurs during the monthly reproductive cycle (to rebuild the uterus lining, to mature the egg during ovulation) and during pregnancy (to build the placenta, the circulation between mother and foetus). The healthy body controls Angiogenesis through a series of 'on' and 'off' switches. The main 'on' switches are known as Angiogenesis-stimulating growth factors. The main 'off' switches are known as Angiogenesis inhibitors. When angiogenic growth factors are produced in excess of angiogenesis inhibitors the balance is tipped in favour of blood vessel growth. When inhibitors are present in excess of stimulators, angiogenesis is stopped. The normal, healthy body maintains a perfect balance of angiogenesis modulators. In general, angiogenesis is 'turned off' by the production of more inhibitors than stimulators. Tumour angiogenesis is the proliferation of a network of blood vessels that penetrates into cancerous growths, supplying nutrients and oxygen and removing waste products. Tumour angiogenesis actually starts with cancerous tumour cells releasing molecules that send signals to surrounding normal host tissue. This signalling activates certain genes in the host tissue that, in turn, cause proteins to encourage growth of new blood vessels. This new book examines its angiogenesis within the context of theory and its applications to cancer treatment.

This new book brings together leading research from around the globe. Leukaemia is a cancer that begins in blood cells. In people with leukaemia, the bone marrow produces abnormal white blood cells. The abnormal cells are leukaemia cells. At first, leukaemia cells function almost normally. In time, they may crowd out normal white blood cells, red blood cells, and platelets. The scope of the book includes the four common types of leukaemia: Chronic lymphocytic leukaemia (chronic lymphoblastic leukaemia, CLL) most often affecting people over age 55. Chronic myeloid leukaemia (chronic myelogenous leukaemia, CML) affects mainly adults. Acute lymphocytic leukaemia (acute lymphoblastic leukaemia, ALL) the most common type of leukaemia in young children. Acute myeloid leukaemia (acute myelogenous leukaemia, AML) which occurs in both adults and children. New advances in diagnosis, pathogenesis and therapy are presented.

With authoritative coverage of rare and common hemostatic disorders, Consultative Hemostasis and Thrombosis, 4th Edition, keeps you both up to date with all that's new in this fast-moving field as well as reviewing background and development and citing pertinent classical literature. Broad differential diagnoses are provided, underscoring the editors' position that correct treatment begins with correct diagnosis. This trusted resource by Drs. Craig S. Kitchens, Craig M. Kessler, Barbara A. Konkle, Michael B. Streiff, and David A. Garcia is designed for rapid reference and critical decision making at the point of care. Emphasizes real-world problems and solutions, with quick access to concise descriptions of each condition, associated symptoms, laboratory findings, differential diagnosis, and treatment. Features a user-friendly design, full-color format, abundant laboratory protocols, and at-a-glance tables and charts throughout. Provides thorough updates on core information on hemostasis and thrombosis, including deep venous thrombosis (DVT), pulmonary embolisms, hypercoagulability, thrombocytopenia, von Willenbrand disease, and more. Covers new treatment information on hemophilia A and B. Contains new chapters on hereditary hemorrhagic telangiectasia, hemolytic uremic syndrome, and paroxymal nocturnal hemoglobinuria. Two new editors, Dr. Michael B. Streiff and Dr. David A. Garcia, offer fresh perspectives and valuable experience. Expert ConsultT eBook version included with purchase. This enhanced eBook experience allows you to search all of the text, figures, and references from the book on a variety of devices.

Neonatal hematology is a fast-growing field, and the majority of sick neonates will develop hematological problems. This is an essential guide to the pathogenesis, diagnosis and management of hematologic problems in the neonate. Guidance is practical, including blood test interpretation, advice on transfusions and reference ranges for hematological values. Chapters have been thoroughly revised according to the latest advances in the field for this updated third edition. Topics discussed include erythrocyte disorders, platelet disorders, leukocyte disorders, immunologic disorders and hemostatic disorders. Coverage of oncological issues has been expanded to two separate chapters on leukemia and solid tumors, making information more easily accessible. Approaches to identifying the cause of anemia in a neonate are explained, with detailed algorithms provided to aid clinicians in practice. Covering an important hematologic niche with an ever increasing amount of specialized knowledge, this book is a valuable resource for hematologists, neonatologists and pediatricians.

This book summarizes current knowledge on chronic lymphocytic leukemia (CLL), taking into account the most recent research. All aspects are considered, including pathophysiology, clinical presentation, diagnosis, prognosis, treatment, follow-up, and complications and their management. Readers will find important information on the various prognostic markers as well as practical guidance on the use of different diagnostic procedures. A key focus of the book is the changing treatment paradigm in CLL as progress in understanding of pathogenesis and pathophysiology leads to the identification of new potential therapeutic targets. General treatment concepts are clearly described, and it is explained how choice of treatment for CLL depends on stage, age, and performance status as well as specific genetic aberrations. In addition, frontline therapeutic strategies for disease relapse, including allogeneic stem cell transplantation, are reported. Looking beyond CLL, the diagnosis and therapy of T-cell prolymphocytic leukemia and T-cell large granular lymphocyte leukemia, two rare CLL-related entities, are addressed.

This volume is the first of its kind to emphasize the visual approach in the diagnosis of cutaneous lymphoid infiltrates. Written and designed in an accessible yet highly detailed format by an expert in the field, this book bridges the knowledge gaps so often found when dealing with skin lymphomas. Complete with more than two hundred high quality images and illustrations, Diagnosis of Cutaneous Lymphoid Infiltrates offers pearls and pitfalls as well as differential diagnoses. Additionally, images are explained and decoded with the use of illustrations and analogies, proving to be an invaluable resource for pathologists, dermatologists, dermatopathologists, hematopathologists, and residents and fellows in these fields.

This clinical casebook covers transfusion medicine theory and its practical implications for the obstetrical hemorrhage patient through the presentation of cases on actively bleeding patients. Each case features a unique clinical scenario involving a bleeding patient and outlines different aspects of safe and effective transfusion support. The cases contain current evidence on the latest topics in the field, such as the use of antifibrinolytic agents and coagulation factor concentrates in the setting of massive obstetrical hemorrhage. In addition to the actively bleeding patient, the casebook includes other important management topics, including the role of plasma exchange in thrombotic microangiopathies during pregnancy; treatment of hyperhemolysis in a patient with hemoglobinopathy; and recommended management of patients with red cell antibodies found on prenatal testing. Other immunohematology topics such as post-natal management of an RhD negative woman for the prevention of hemolytic disease of the newborn due to anti-Rh(D) are included. Written by transfusion medicine, coagulation, obstetrical, and anesthesiology experts, Transfusion Management of the Obstetrical Patient: A Clinical Casebook is a concise yet comprehensive resource for anesthesiologists, obstetricians, pathologists, hematologists, and other practitioners who treat obstetrical hemorrhage patients.