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1
L, Nagel R., ed. Genetically abnormal red cells. Boca Raton, Fla: CRC Press, 1988.
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2
A, Tanner M. J., and Anstee D. J, eds. Red cell membrane disorders. London: Baillière Tindall, 1999.
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3
A, Zanella, ed. Inherited disorders of red cell metabolism. London: Baillière Tindall, 2000.
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4
R, Bridges Kenneth, and Pearson Howard A, eds. Anemias and other red cell disorders. New York: McGraw-Hill, 2007.
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5
Alberto, Zanella, ed. Inherited disorders of red cell metabolism. London: Baillière Tindall, 2000.
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6
Malaria resistance or susceptibility in red cells disorders. Hauppauge, NY: Nova Science, 2009.
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7
1915-, Finch Clement A., ed. Red cell manual. 7th ed. Philadelphia: F.A. Davis, 1996.
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8
1915-, Finch Clement A., ed. Red cell manual. 5th ed. Philadelphia: F.A. Davis, 1985.
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9
Hillman, Robert S. Red cell manual. 6th ed. Philadelphia: F.A. Davis, 1992.
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10
Tsuyoshi, Ohnishi S., and Ohnishi Tomoko, eds. Membrane abnormalities in sickle cell disease and in other red blood cell disorders. Boca Raton, Fla: CRC Press, 1994.
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11
1949-, Agre Peter, and Parker John C. 1935-, eds. Red blood cell membranes: Structure, function, clinical implications. New York: Dekker, 1989.
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12
Provan, Drew, Trevor Baglin, Inderjeet Dokal, and Johannes de Vos. Red cell disorders. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199683307.003.0002.
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The peripheral blood film in anaemias - Anaemia in renal disease - Anaemia in endocrine disease - Anaemia in joint disease - Anaemia in gastrointestinal disease - Anaemia in liver disease - Iron (Fe) deficiency anaemia - Vitamin B12 deficiency - Folate deficiency - Other causes of megaloblastic anaemia - Anaemia in other deficiency states - Haemolytic syndromes - Genetic control of haemoglobin production - Sickling disorders - HbS—sickle-modifying therapies - Sickle cell trait (HbAS) - Other sickling disorders - Other haemoglobinopathies - Unstable haemoglobins - Thalassaemias - α thalassaemia - β thalassaemia - Other thalassaemias - Hereditary persistence of fetal haemoglobin - Hb patterns in haemoglobin disorders - Non-immune haemolysis - Hereditary spherocytosis - Hereditary elliptocytosis - Glucose-6-phosphate dehydrogenase (G6PD) deficiency - Pyruvate kinase deficiency - Other red cell enzymopathies - Drug-induced haemolytic anaemia - Methaemoglobinaemia - Microangiopathic haemolytic anaemia - Acanthocytosis - Autoimmune haemolytic anaemia - Cold haemagglutinin disease - Leucoerythroblastic anaemia - Aplastic anaemia - Paroxysmal nocturnal haemoglobinuria - Pure red cell aplasia - Iron (Fe) overload - Transfusion haemosiderosis
13
Provan, Drew, Trevor Baglin, Inderjeet Dokal, Johannes de Vos, Banu Kaya, and Angela Theodoulou. Red cell disorders. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199683307.003.0002_update_001.
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The peripheral blood film in anaemias - Anaemia in renal disease - Anaemia in endocrine disease - Anaemia in joint disease - Anaemia in gastrointestinal disease - Anaemia in liver disease - Iron (Fe) deficiency anaemia - Vitamin B12 deficiency - Folate deficiency - Other causes of megaloblastic anaemia - Anaemia in other deficiency states - Haemolytic syndromes - Genetic control of haemoglobin production - Sickling disorders - HbS—sickle-modifying therapies - Sickle cell trait (HbAS) - Other sickling disorders - Other haemoglobinopathies - Unstable haemoglobins - Thalassaemias - α thalassaemia - β thalassaemia - Other thalassaemias - Hereditary persistence of fetal haemoglobin - Hb patterns in haemoglobin disorders - Non-immune haemolysis - Hereditary spherocytosis - Hereditary elliptocytosis - Glucose-6-phosphate dehydrogenase (G6PD) deficiency - Pyruvate kinase deficiency - Other red cell enzymopathies - Drug-induced haemolytic anaemia - Methaemoglobinaemia - Microangiopathic haemolytic anaemia - Acanthocytosis - Autoimmune haemolytic anaemia - Cold haemagglutinin disease - Leucoerythroblastic anaemia - Aplastic anaemia - Paroxysmal nocturnal haemoglobinuria - Pure red cell aplasia - Iron (Fe) overload - Transfusion haemosiderosis
14
Bunch, Chris. Haemolytic anaemia. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0280.
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Haemolytic anaemias occur when the rate of red-cell breakdown is increased and exceeds the marrow’s capacity to generate new cells. Increased red-cell destruction, or haemolysis, may reflect a broad range of disorders. Some involve intrinsic defects in the red cell itself; in others, the red cells are normal but are subjected to external factors which lead to premature destruction. Many of the intrinsic defects are due to inherited disorders affecting the red-cell membrane, its enzymes, or haemoglobin. The marrow can normally compensate for moderate haemolysis by increasing red-cell production up to tenfold. Only when haemolysis is severe and the red-cell lifespan is reduced to less than about 15 days, or the marrow is unable to compensate, will anaemia occur. This chapter addresses the diagnosis, investigation, and management of haemolytic anaemias, including hereditary spherocytosis, paroxysmal nocturnal haemoglobinuria, glucose-6-phosphate dehydrogenase deficiency, haemoglobinopathies, and mechanical and immune haemolytic anaemias.
15
Lance, Eboni I., and Andrew W. Zimmerman. Sickle Cell Anemia. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0079.
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Sickle cell disease is a genetic hematological disorder involving red blood cells that become deformed when stressed. Patients with homozygous hemoglobin SS disease often have multiple systemic and neurologic complications, particularly stroke. Intellectual disability is commonly seen in the population, in patients with and without a history of stroke, attributed to different underlying mechanisms of brain injury. Autism is rare and not described in sickle cell disease in the literature to date. Many treatments (chronic transfusion therapy, hydroxyurea, bone marrow transplant) are in trials at this time to see if risk of stroke and other neurologic complications can be reduced (ClinicalTrials.gov identifiers: NCT01425307, NCT01389024, NCT00152113).
16
Bridges, Kenneth. Anemias and Other Red Cell Disorders. McGraw-Hill Professional, 2007.
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17
Bridges, Kenneth. Anemias and Other Red Cell Disorders. McGraw-Hill Professional, 2007.
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18
Mettananda, Sachith. Guide to Paediatric Red Blood Cell Disorder. Nova Science Publishers, Incorporated, 2020.
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19
Mettananda, Sachith. Guide to Paediatric Red Blood Cell Disorder. Nova Science Publishers, Incorporated, 2020.
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20
Hemolytic Anemia in Disorders of Red Cell Metabolism. Springer, 2012.
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21
Lindbergh, Ernest. Hemolytic Anemia in Disorders of Red Cell Metabolism. Springer, 2012.
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22
Buetler, Ernest. Hemolytic Anemia in Disorders of Red Cell Metabolism. Springer, 2012.
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23
Collins, Graham, and Chris Bunch. Myeloproliferative disorders. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0291.
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Myeloproliferative disorders (also called myeloproliferative neoplasms) can be defined as clonal haematopoietic disorders resulting in excess production of one or more blood cell lineage. The four main conditions are primary polycythaemia, which is characterized by excess red-cell production; essential thrombocythaemia, which is characterized by excess platelet production; chronic myeloid leukaemia, which is characterized by excess granulocyte production; and myelofibrosis, which is characterized by excess megakaryocyte proliferation, which results in a reactive fibroblast proliferation causing marrow fibrosis and failure. This chapter addresses the causes, diagnosis, and management of these myeloproliferative disorders.
24
(Editor), I. Bernhardt, and J. C. Ellory (Editor), eds. Red Cell Membrane Transport in Health and Disease. Springer, 2003.
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25
Collins, Graham, and Chris Bunch. Lymphoma. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0289.
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Lymphoma is a cancerous disorder characterized by a clonal proliferation of lymphocytes. There are two broad categories: Hodgkin’s lymphoma, and non-Hodgkin’s lymphoma, with Hodgkin’s lymphoma defined by the presence of Reed–Sternberg cells on histological examination of affected tissue. Within the non-Hodgkin’s lymphomas, there are the much more common B-cell lymphomas and the uncommon T-cell lymphomas. Within the B-cell non-Hodgkin lymphomas, there are clinically aggressive (high-grade) forms and much more indolent (low-grade) forms. This chapter addresses the causes, diagnosis, and management of Hodgkin’s lymphoma and non-Hodgkin’s lymphoma.
26
Provan, Drew, Trevor Baglin, Inderjeet Dokal, and Johannes de Vos. Paediatric haematology. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199683307.003.0012.
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Blood counts in children - Red cell transfusion and blood component therapy—special considerations in neonates and children - Polycythaemia in newborn and childhood - Neonatal anaemia - Anaemia of prematurity - Haemolytic anaemia in the neonate - Congenital red cell defects - Acquired red cell defects - Haemolytic disease of the newborn - Hyperbilirubinaemia - Neonatal haemostasis - Neonatal alloimmune thrombocytopenia - Congenital dyserythropoietic anaemias - Congenital red cell aplasia - Acquired red cell aplasia - Fanconi anaemia - Rare congenital marrow failure syndromes - Neutropenia in childhood - Disorders of neutrophil function - Childhood immune (idiopathic) thrombocytopenic purpura - Haemolytic uraemic syndrome - Childhood cancer and malignant blood disorders - Childhood lymphoblastic leukaemia - Childhood lymphomas - Childhood acute myeloid leukaemia - Childhood myelodysplastic syndromes and chronic leukaemias - Histiocytic syndromes - Haematological effects of systemic disease in children
27
Provan, Drew, Trevor Baglin, Inderjeet Dokal, Johannes de Vos, and Angela Theodoulou. Paediatric haematology. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199683307.003.0012_update_001.
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Blood counts in children - Red cell transfusion and blood component therapy—special considerations in neonates and children - Polycythaemia in newborn and childhood - Neonatal anaemia - Anaemia of prematurity - Haemolytic anaemia in the neonate - Congenital red cell defects - Acquired red cell defects - Haemolytic disease of the newborn - Hyperbilirubinaemia - Neonatal haemostasis - Neonatal alloimmune thrombocytopenia - Congenital dyserythropoietic anaemias - Congenital red cell aplasia - Acquired red cell aplasia - Fanconi anaemia - Rare congenital marrow failure syndromes - Neutropenia in childhood - Disorders of neutrophil function - Childhood immune (idiopathic) thrombocytopenic purpura - Haemolytic uraemic syndrome - Childhood cancer and malignant blood disorders - Childhood lymphoblastic leukaemia - Childhood lymphomas - Childhood acute myeloid leukaemia - Childhood myelodysplastic syndromes and chronic leukaemias - Histiocytic syndromes - Haematological effects of systemic disease in children
28
Bunch, Chris. Normal blood function. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0277.
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This chapter reviews normal blood function and disorders of haemopoiesis. Blood consists of cells of three main types, suspended in plasma. The cellular component comprises about 40%–50% of the total volume and consists of red cells (erythrocytes), white cells (leucocytes), and platelets. Blood cells are formed from progenitor cells in the bone marrow by haemopoiesis, a process of proliferation and differentiation. Failure of haemopoiesis usually results from damage to proliferating marrow cells by cytotoxic drugs or radiation, haemopoietic malignancy, or a combination of the two.
29
Monoclonal antibodies against human red blood cell and related antigens. Paris: Arnette, 1988.
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30
Bunch, Chris. Splenomegaly and other disorders of the spleen. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0035.
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The spleen is a predominantly lymphoid organ, normally about the size of a clenched fist located beneath the diaphragm in the left upper abdomen. It has a dual role as a filter for the circulation, and a primary lymphoid organ in its own right. About three-quarters of its volume is a matrix of capillaries and sinuses (the red pulp), through which blood is able to percolate slowly and come into contact with fixed macrophages, which are able to remove senescent or damaged red cells, or other particulate matter such as bacteria. The lymphoid tissue is organized into scattered follicles (the white pulp), which have a particularly important role in initiating primary humoral immune responses and antibody (IgM) synthesis. The spleen commonly enlarges when either its filtration function is increased—as in haemolysis—or it is stimulated by infection or inflammation. It may also be involved in myeloproliferative and lymphoproliferative neoplasias. This chapter covers hypersplenism, splenectomy, hyposplenism, overwhelming post-splenectomy infection (OPSI), and other infections in hyposplenic patients.
31
Albert, Tyler J., and Erik R. Swenson. The blood cells and blood count. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0265.
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Blood is a dynamic fluid consisting of cellular and plasma components undergoing constant regeneration and recycling. Like most physiological systems, the concentrations of these components are tightly regulated within narrow limits under normal conditions. In the critically-ill population, however, haematological abnormalities frequently occur and are largely due to non-haematological single- or multiple-organ pathology. Haematopoiesis originates from the pluripotent stem cell, which undergoes replication, proliferation, and differentiation, giving rise to cells of the erythroid, myeloid, and lymphoid series, as well as megakaryocytes, the precursors to platelets. The haemostatic system is responsible for maintaining blood fluidity and, at the same time, prevents blood loss by initiating rapid, localized, and appropriate blood clotting at sites of vascular damage. This system is complex, comprising both cellular and plasma elements, i.e. platelets, coagulation and fibrinolytic cascades, the natural intrinsic and extrinsic pathways of anticoagulation, and the vascular endothelium. A rapid, reliable, and inexpensive method of examining haematological disorders is the peripheral blood smear, which allows practitioners to assess the functional status of the bone marrow during cytopenic states. Red blood cells, which are primarily concerned with oxygen and carbon dioxide transport, have a normal lifespan of only 120 days and require constant erythropoiesis. White blood cells represent a summation of several circulating cell types, each deriving from the hematopoietic stem cell, together forming the critical components of both the innate and adaptive immune systems. Platelets are integral to haemostasis, and also aid our inflammatory and immune responses, help maintain vascular integrity, and contribute to wound healing.
32
Mannucci, Pier Mannuccio, and Maddalena Lettino. Bleeding and haemostasis disorders. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0070_update_003.
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The main cause of haemostasis defects and related bleeding complications in patients with acute coronary syndromes admitted to the intensive cardiac care unit is the use of multiple antithrombotic drugs, alone or concomitantly with invasive procedures such as percutaneous coronary intervention with stent deployment and coronary artery bypass surgery. These drugs, that act upon several components of haemostasis (platelet function, coagulation, fibrinolysis), are associated with bleeding complications, particularly in elderly patients (more so in women than in men), those who are underweight, and those with comorbid conditions such as renal and liver insufficiency and diabetes. The identification of patients at higher risk of bleeding is the most important preventive strategy. Red cell and platelet transfusions, which may become necessary in patients with severe bleeding, should be used with caution, because transfused patients with acute coronary syndrome have a high rate of adverse outcomes (death, myocardial infarction, and stroke).
33
Mannucci, Pier Mannuccio. Bleeding and haemostasis disorders. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0070.
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The main cause of haemostasis defects and related bleeding complications in patients with acute coronary syndromes admitted to the intensive cardiac care unit is the use of multiple antithrombotic drugs, alone or concomitantly with invasive procedures such as percutaneous coronary intervention with stent deployment and coronary artery bypass surgery. These drugs, that act upon several components of haemostasis (platelet function, coagulation, fibrinolysis), are associated with bleeding complications, particularly in elderly patients (more so in women than in men), those who are underweight, and those with comorbid conditions such as renal and liver insufficiency and diabetes. The identification of patients at higher risk of bleeding is the most important preventive strategy. Red cell and platelet transfusions, which may become necessary in patients with severe bleeding, should be used with caution, because transfused patients with acute coronary syndrome have a high rate of adverse outcomes (death, myocardial infarction, and stroke). To reduce the need of transfusion, haemostatic agents that decrease blood loss and transfusion requirements (antifibrinolytic amino acids, plasmatic prothrombin complex concentrates, recombinant factor VIIa) may be considered. However, the efficacy of these agents in the control of bleeding complications in acute coronary syndrome is not unequivocally established, and there is concern for an increased risk of re-thrombosis. A low platelet count is another cause of bleeding in the intensive cardiac care unit. The main aetiologies are drugs (unfractionated heparin and glycoprotein IIb/IIIa inhibitors), thrombotic microangiopathies, such as thrombotic thrombocytopenic purpura, and disseminated intravascular coagulation, that are often paradoxically associated with thrombotic manifestations. In conclusion, evidence-based recommendations for the management of bleeding in patients admitted to the intensive cardiac care unit are lacking. Accurate assessments of the risk of bleeding in the individual and prevention measures are the most valid strategies.
34
Mannucci, Pier Mannuccio. Bleeding and haemostasis disorders. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199687039.003.0070_update_001.
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The main cause of haemostasis defects and related bleeding complications in patients with acute coronary syndromes admitted to the intensive cardiac care unit is the use of multiple antithrombotic drugs, alone or concomitantly with invasive procedures such as percutaneous coronary intervention with stent deployment and coronary artery bypass surgery. These drugs, that act upon several components of haemostasis (platelet function, coagulation, fibrinolysis), are associated with bleeding complications, particularly in elderly patients (more so in women than in men), those who are underweight, and those with comorbid conditions such as renal and liver insufficiency and diabetes. The identification of patients at higher risk of bleeding is the most important preventive strategy. Red cell and platelet transfusions, which may become necessary in patients with severe bleeding, should be used with caution, because transfused patients with acute coronary syndrome have a high rate of adverse outcomes (death, myocardial infarction, and stroke). To reduce the need of transfusion, haemostatic agents that decrease blood loss and transfusion requirements (antifibrinolytic amino acids, plasmatic prothrombin complex concentrates, recombinant factor VIIa) may be considered. However, the efficacy of these agents in the control of bleeding complications in acute coronary syndrome is not unequivocally established, and there is concern for an increased risk of re-thrombosis. A low platelet count is another cause of bleeding in the intensive cardiac care unit. The main aetiologies are drugs (unfractionated heparin and glycoprotein IIb/IIIa inhibitors), thrombotic microangiopathies, such as thrombotic thrombocytopenic purpura, and disseminated intravascular coagulation, that are often paradoxically associated with thrombotic manifestations. In conclusion, evidence-based recommendations for the management of bleeding in patients admitted to the intensive cardiac care unit are lacking. Accurate assessments of the risk of bleeding in the individual and prevention measures are the most valid strategies.
35
Mannucci, Pier Mannuccio. Bleeding and haemostasis disorders. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0070_update_002.
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The main cause of haemostasis defects and related bleeding complications in patients with acute coronary syndromes admitted to the intensive cardiac care unit is the use of multiple antithrombotic drugs, alone or concomitantly with invasive procedures such as percutaneous coronary intervention with stent deployment and coronary artery bypass surgery. These drugs, that act upon several components of haemostasis (platelet function, coagulation, fibrinolysis), are associated with bleeding complications, particularly in elderly patients (more so in women than in men), those who are underweight, and those with comorbid conditions such as renal and liver insufficiency and diabetes. The identification of patients at higher risk of bleeding is the most important preventive strategy. Red cell and platelet transfusions, which may become necessary in patients with severe bleeding, should be used with caution, because transfused patients with acute coronary syndrome have a high rate of adverse outcomes (death, myocardial infarction, and stroke). To reduce the need of transfusion, haemostatic agents that decrease blood loss and transfusion requirements (antifibrinolytic amino acids, plasmatic prothrombin complex concentrates, recombinant factor VIIa) may be considered. However, the efficacy of these agents in the control of bleeding complications in acute coronary syndrome is not unequivocally established, and there is concern for an increased risk of re-thrombosis. A low platelet count is another cause of bleeding in the intensive cardiac care unit. The main aetiologies are drug usage (unfractionated heparin and glycoprotein IIb/IIIa inhibitors), such thrombotic microangiopathies as thrombotic thrombocytopenic purpura and disseminated intravascular coagulation, that are often paradoxically associated with thrombotic manifestations. In conclusion, evidence-based recommendations for the management of bleeding in patients admitted to the intensive cardiac care unit are lacking. Accurate assessments of the risk of bleeding in the individual and prevention measures are the most valid strategies.
36
Spinella, Philip C., and Jeffrey J. Bednarski. Hematology and Oncology. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199918027.003.0013.
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Coagulopathy, thrombosis, and other hematological abnormalities are common in the pediatric intensive care unit . Current guidelines recommend red blood cell transfusion for a hemoglobin concentration less than 7 g/dL in critically ill, hemodynamically stable patients; platelets for a concentration less than 10,000 in nonbleeding patients; and cryoprecipitate in bleeding patients for fibrinogen values less than 100 to 150 mg/dL. Massive transfusion protocols that push blood products to the bedside are more practical than reactive protocols. Transfusion reactions include transfusion-associated acute lung injury and transfusion-associated circulatory overload. Hematologic crises in the PICU are commonly complications of other primary disorders. Sickle cell disease may lead to acute chest syndrome, sequestration crisis, and stroke, and require aggressive intervention. Oncological diseases produce hyperleukocytosis, tumor lysis syndrome, veno-occlusive disease, graft-versus-host disease, and sepsis in association with leukopenia. A relatively newly recognized disorder, hemophagocytic lymphohistiocytosis, requires early recognition and treatment to avoid adverse outcomes.
37
Gluckman, Sir Peter, Mark Hanson, Chong Yap Seng, and Anne Bardsley. Vitamin B9 (folate) in pregnancy and breastfeeding. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198722700.003.0012.
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Folate is a coenzyme in multiple biochemical pathways involving one-carbon metabolism, including amino acid metabolism, DNA and RNA synthesis, homocysteine metabolism, and methylation of DNA. The most overt consequence of folate deficiency is megaloblastic anaemia caused by the inhibition of DNA synthesis in red blood cell production. Folate deficiency may also influence the ability to maintain DNA methylation patterns in replicating cells, resulting in lasting phenotypic changes. Embryogenesis and fetal growth require higher levels of folate, which must be supplied maternally during pregnancy. A link between low maternal folate levels and the occurrence of neural tube defects has long been recognized. Other effects in pregnancy include increased risks of pre-eclampsia and placental vascular disorders. The general recommendation is for supplementation prior to conception and throughout pregnancy with 400 #amp;#x03BC;g of folic acid in tablet form, in addition to dietary sources, which can reduce the risk of neural tube defects.
38
Bunch, Chris. Myelodysplasia. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0288.
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The myelodysplastic syndromes (or myelodysplasias) comprise a spectrum of disorders characterized by dysplastic or ineffective haemopoiesis that leads to variable anaemia, neutropenia, and thrombocytopenia. There is often a degree of red-cell macrocytosis. The majority are clonal stem cell disorders in which the abnormal clone predominates and expands only slowly over a number of years. Myelodysplasias have a tendency to develop ultimately into acute leukaemia in some patients; for this reason, they are sometimes referred to as ‘preleukaemias’, even though two-thirds of patients will never develop this complication. This chapter addresses the causes, diagnosis, and management of myelodysplastic syndromes.
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Hendriks, Herman G. D., and Joost T. M. de Wolf. Haematological and coagulation disorders and anaesthesia. Edited by Philip M. Hopkins. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0084.
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This chapter covers the principal haematological disorders and their implications for anaesthesia. Haemoglobin concentration is the main determinant of oxygen delivery to the tissues making anaemia a potential concern for the anaesthetist. In deciding whether to correct anaemia with a red blood cell transfusion, the anaesthetist must consider the nature of the surgery and the underling cause of the anaemia as well as the haemoglobin concentration. Techniques to limit the need for blood transfusion and the complications of transfusion are discussed. Perfect haemostasis means control of bleeding without the occurrence of thrombotic events. Coagulation management requires an understanding of this balance and the knowledge that altered coagulation activity may result in clinically relevant bleeding or, in contrast, thrombosis. Therefore, the key in haemostasis is an understanding that every anticoagulant action enhances the risk of bleeding and every procoagulant action enhances the risk of thrombosis. If a specific defect in the haemostatic system is known, treatment is tailored to restore this defect. However, tests to predict surgical bleeding do not exist, as it is for test to predict thrombotic events. The strengths and limitations of coagulation tests should be appreciated before they are used to assist clinical decision-making in the perioperative period. An excellent coagulation test is the clinical field (i.e. the surgical wound). If there are abnormalities in the coagulation tests without clinical bleeding, a correction is hardly necessary. In patients taking anticoagulant medication, consideration must be given on an individual patient basis, to the relative risks of continuing (bleeding) or stopping (thrombotic events) the medication.
40
Steensma, David P. Benign Hematology. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0294.
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The major forms of benign hematologic conditions are anemia, neutropenia, transfusion reactions, Gaucher disease, and porphyria. Anemia is a sign of disease rather than a disease itself. Anemia results from 1 or more of 3 pathologic mechanisms: inadequate production of red blood cells (RBCs) by the bone marrow, blood loss, or premature destruction of RBCs. The major causes of neutropenia include hematologic neoplasm, metastatic neoplasm involving the marrow, irradiation, vitamin B12 deficiency and folate deficiency, drugs, infections, congenital or acquired primary disorders of hematopoiesis, autoimmune neutropenia, hypersplenism, hemodilution, and benign idiopathic neutropenia. The porphyrias are enzyme disorders that are autosomal dominant with low disease penetrance, except for congenital erythropoietic porphyria, which is autosomal recessive, and porphyria cutanea tarda, which may be acquired and is associated with hepatitis C and hemochromatosis.