Книги: "Thrombotic complications"

1

Hans, Renck, ed. Bleeding and thrombotic disorders in the surgical patient. Norwalk, Conn: Appleton & Lange, 1988.

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2

Gilles, Lugassy, ed. Thrombosis and cancer. London: Martin Dunitz, 2004.

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3

Greco, Caterina F. Stent thrombosis: Epidemiology, prevention, and management. Hauppauge, N.Y: Nova Science, 2011.

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4

Paidas, Michael J. Hemostasis and thrombosis in obstetrics & gynecology. Chichester, West Sussex, UK: Wiley-Blackwell, 2011.

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5

International School of Medical Sciences (22nd 1983 Ettore Majorana Center for Scientific Culture). Advances in hemostasis and thrombosis. New York: Plenum Press, 1985.

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6

Valentin, Fuster, and Verstraete M, eds. Thrombosis in cardiovascular disorders. Philadelphia: Saunders, 1992.

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7

Bodnar, Endre, and Eric G. Butchart. Thrombosis, embolism and bleeding. London: ICR Publ., 1992.

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8

Wang, Meng-Jiy. Biomaterials in blood-contacting devices: Complications and solutions. New York: Nova Science Publishers, 2010.

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9

M, Verstraete, Fuster Valentin, and Topol Eric J. 1954-, eds. Cardiovascular thrombosis: Thrombocardiology and thromboneurology. 2nd ed. Philadelphia: Lippincott-Raven, 1998.

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10

1958-, Greer I. A., Turpie, A. G. G. 1939-, and Forbes C. D. 1938-, eds. Haemostasis and thrombosis in obstetrics and gynaecology. London: Chapman & Hall Medical, 1992.

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11

Wang, Meng-Jiy. Biomaterials in blood-contacting devices: Complications and solutions. Hauppauge, N.Y: Nova Science Publishers, 2009.

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12

Benjamin, Brenner, Marder Victor J, and Conard Jacqueline, eds. Women's issues in thrombosis and hemostasis. London: Martin Dunitz, 2002.

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13

Greer, I. A. Venous thrombosis in women: Pregnancy, the contraceptive pill, and hormone replacement therapy / I.A. Greer. Boca Raton: Parthenon Pub., 2003.

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14

J, Seghatchian M., Samama Meyer M, and Hecker S. P, eds. Hypercoagulable states: Fundamental aspects, acquired disorders, and congenital thrombophilia. Boca Raton: CRC Press, 1996.

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15

Becker, Richard C. Fibrinolytic and antithrombotic therapy: Theory, practice, and management. 2nd ed. New York: Oxford University Press, 2006.

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16

Becker, Richard C. Fibrinolytic and antithrombotic therapy: Theory, practice, and management. 2nd ed. New York, NY: Oxford University Press, 2005.

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17

I, Schafer Andrew, ed. Molecular mechanisms of hypercoagulable states. New York: Chapman & Hall, 1997.

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18

1956-, Calligaro Keith D., DeLaurentis Dominic A, and Baker William Henry 1937-, eds. Management of extracranial cerebrovascular disease. Philadelphia: Lippincott-Raven, 1997.

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19

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.

20

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.

21

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.

22

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.

23

Irani, Zubin, and Sara Zhao. Dual and Balloon-Assisted AngioJet Thrombectomy for Iliofemoral Deep Venous Thrombosis. Edited by S. Lowell Kahn, Bulent Arslan, and Abdulrahman Masrani. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199986071.003.0038.

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Lower extremity deep venous thrombosis (DVT) may be complicated by pulmonary embolism, post-thrombotic syndrome, and phlegmasia cerulea dolens. Due to these complications, the American Venous Forum now recommends thrombus removal for large or symptomatic thrombus burden. The AngioJet Solent Proxy and Omni thrombectomy sets are indicated for use in iliofemoral and lower extremity veins with a diameter ≥3 mm. The device has quickly become a preferred device among the available mechanical thrombectomy options. The AngioJet system has been demonstrated as both efficacious and safe as a method of thrombectomy in lower extremity DVT. This chapter discusses two techniques to utilize the AngioJet device in iliofemoral DVT.

24

Khamashta, Munther A., Graham R. V. Hughes, and Guillermo Ruiz-Irastorza. Anti-phospholipid antibody syndrome. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0120.

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The anti-phospholipid syndrome (APS) described almost 30 years ago, is now recognized as a major cause of deep vein thrombosis, stroke, and heart attacks in young people (<45 years of age). It is also the commonest treatable cause of recurrent miscarriages and a major cause of late fetal death. Other clinical manifestations are cardiac valvular disease, livedo reticularis, renal thrombotic microangiopathy, thrombocytopenia, haemolytic anaemia, epilepsy, and cognitive impairment. The presence of anti-phospholipid antibodies (aPL) has been closely related to the development of thrombosis and complications in pregnancy. However, not all patients with aPL will develop the clinical features. Lupus anticoagulant is generally thought to be more strongly associated with the risk of clinical manifestations of APS than anticardiolipin and anti ?2-glycoprotein I antibodies. The exact pathogenic mechanisms leading to thrombosis and/or pregnancy morbidity are poorly understood. Therapy of thrombosis is based on long-term oral anti-coagulation and patients with arterial events should be treated aggressively. Obstetric care is based on combined medical-obstetric high-risk management and treatment with aspirin and heparin.

25

Khamashta, Munther A., Graham R. V. Hughes, and Guillermo Ruiz-Irastorza. Anti-phospholipid antibody syndrome. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199642489.003.0120_update_001.

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The anti-phospholipid syndrome (APS) described almost 30 years ago, is now recognized as a major cause of deep vein thrombosis, stroke, and heart attacks in young people (<45 years of age). It is also the commonest treatable cause of recurrent miscarriages and a major cause of late fetal death. Other clinical manifestations are cardiac valvular disease, livedo reticularis, renal thrombotic microangiopathy, thrombocytopenia, haemolytic anaemia, epilepsy, and cognitive impairment. The presence of anti-phospholipid antibodies (aPL) has been closely related to the development of thrombosis and complications in pregnancy. However, not all patients with aPL will develop the clinical features. Lupus anticoagulant is generally thought to be more strongly associated with the risk of clinical manifestations of APS than anticardiolipin and anti ?2-glycoprotein I antibodies. The exact pathogenic mechanisms leading to thrombosis and/or pregnancy morbidity are poorly understood. Therapy of thrombosis is based on long-term oral anti-coagulation and patients with arterial events should be treated aggressively. Obstetric care is based on combined medical-obstetric high-risk management and treatment with aspirin and heparin.

26

Cheong, Adrian, Gabriel Steg, and Stefan K. James. ST-segment elevation myocardial infarction. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0043.

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Acute myocardial infarction with ST-segment elevation is a common and dramatic manifestation of coronary artery disease. It is caused by the rupture of an atherosclerotic plaque in a coronary artery, leading to its total thrombotic occlusion and resultant ischaemia and necrosis of downstream myocardium. The diagnosis of ST-segment elevation myocardial infarction is based on a syndrome of ischaemic chest pain symptoms, associated with typical ST-segment elevation on the electrocardiogram and an eventual rise in biomarkers of myocardial necrosis. The treatment of ST-segment elevation myocardial infarction is focused on re-establishing blood flow in the coronary artery involved, preferably by percutaneous coronary intervention, or by pharmacological thrombolysis in the case of expected lengthy time delays or lack of availability of facilities. Early mortality from ST-segment elevation myocardial infarction can be attributed to the sequelae or complications of myocardial ischaemia, or complications related to therapy. The former include arrhythmias (such as ventricular tachycardia or fibrillation), mechanical complications (such as ventricular free wall, septal, and mitral chordal rupture), and pump failure leading to cardiogenic shock. The latter includes haemorrhagic complications and coronary stent thrombosis. Given that myocardial necrosis is a critically time-dependent process, the organization of an ST-segment elevation myocardial infarction care system and adherence to the latest clinical trial evidence and guidelines are crucial to ensure that patients are treated in an optimal manner.

27

Cheong, Adrian P., Gabriel Steg, and Stefan K. James. ST-segment elevation MI. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0043_update_001.

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Acute myocardial infarction with ST-segment elevation is a common and dramatic manifestation of coronary artery disease. It is caused by the rupture of an atherosclerotic plaque in a coronary artery, leading to its total thrombotic occlusion and resultant ischaemia and necrosis of downstream myocardium. The diagnosis of ST-segment elevation myocardial infarction is based on a syndrome of ischaemic chest pain symptoms, associated with typical ST-segment elevation on the electrocardiogram and an eventual rise in biomarkers of myocardial necrosis. The treatment of ST-segment elevation myocardial infarction is focused on re-establishing blood flow in the coronary artery involved, preferably by percutaneous coronary intervention, or by pharmacological thrombolysis in the case of expected lengthy time delays or lack of availability of facilities. Early mortality from ST-segment elevation myocardial infarction can be attributed to the sequelae or complications of myocardial ischaemia, or complications related to therapy. The former include arrhythmias (such as ventricular tachycardia or fibrillation), mechanical complications (such as ventricular free wall, septal, and mitral chordal rupture), and pump failure leading to cardiogenic shock. The latter includes haemorrhagic complications and coronary stent thrombosis. Given that myocardial necrosis is a critically time-dependent process, the organization of an ST-segment elevation myocardial infarction care system and adherence to the latest clinical trial evidence and guidelines are crucial to ensure that patients are treated in an optimal manner.

28

Lip, Gregory Y. H., and Andrew D. Blann. ABC of Antithrombotic Therapy (ABC). Blackwell Publishing Limited, 2003.

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29

Lip, Gregory Y. H., and Andrew Blann. ABC of Antithrombotic Therapy. Wiley & Sons, Incorporated, John, 2008.

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30

Venous Thrombosis: Risk Factors, Management and Complications. Nova Science Pub Inc, 2014.

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31

Rajakrishna, Premil, Stewart Cameron, and Neil Turner. Nephrotic syndrome. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0052.

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Nephrotic syndrome is the constellation of manifestations seen in patients with such severe proteinuria that serum albumin falls below normal levels. Its severity and the risk of complications are graded by the severity of the protein loss. The risks of some complications begin to rise at levels of proteinuria below those conventionally associated with nephrotic syndrome. The main manifestation, oedema, is characterized by avid sodium retention and managed by sodium restriction and diuretics. A pronounced thrombotic tendency is particularly apparent within the first 6 months of diagnosis and in patients with the most severe proteinuria. Venous thromboembolism may be a presenting feature. Prophylactic full anticoagulation may be considered for those at highest risk. Hyperlipidaemia is severe and justifies lipid-lowering therapy in patients with sustained nephrotic syndrome. There is a marked increased risk of bacterial infection, particularly from Streptococcus pneumoniae. The causes of nephrotic syndrome are diseases affecting the podocyte, either directly or through an effect on glomerular matrix (e.g. through scarring). Identification of a cause is important for management and often requires a renal biopsy.

32

Dragun, Duska, and Björn Hegner. Acute kidney injury in pregnancy. Edited by Norbert Lameire. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0250_update_001.

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Any kind of acute renal deterioration that occurs in young women may, besides typical pregnancy-related disorders, account for pregnancy-related acute kidney injury (PR-AKI). Incidence of PR-AKI is continuously decreasing, yet still represents a significant cause of fetomaternal morbidity and mortality. Hyperemesis gravidarum causing volume depletion and septic shock with renal cortical necrosis upon septic abortion are major causes of PR-AKI during early pregnancy. Pre-eclampsia and bleeding complications associated with placental abruption or other causes of obstetric haemorrhage are responsible for the majority of cases during late pregnancy (after week 35) and puerperium. Haemolytic uraemic syndrome and thrombotic thrombocytopenic purpura disorders are less common than pre-eclampsia, yet represent a diagnostic and therapeutic challenge due to similar features to severe pre-eclampsia cases.

33

Morava, Eva, and Mirian C. H. Janssen. Congenital Disorders of Glycosylation. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0063.

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Congenital disorders of glycosylation (CDGs) are usually diagnosed during infancy or childhood with severe multisystem disorder and neurologic presentation. With the increasing number of surviving adult patients, recognition of the distinct adult phenotype and awareness of the diagnostic difficulties in adulthood is essential. Patients with O-glycosylation defects or with abnormal dolichol synthesis might present first in adulthood. The majority of cases with adult CDG have a neurologic disease with intellectual disability, ataxia, speech disorder, visual disturbance, and skeletal findings. Psychological abnormalities are also common. Thrombotic complications and endocrine dysfunction might persist to adulthood. MPI-CDG, the only treatable form of CDG, might progress to chronic liver failure. Genetic testing is recommended in suspected cases, since transferrin screening analysis can be normal in adults, even in N-linked glycosylation disorders.

34

Wilson-MacDonald, James, and Andrew James. Complications of fractures. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199550647.003.012002.

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♦ Fat embolism syndrome is defined as the presence of globules of fat in the lungs and in other tissues and occurs occasionally in long bone fractures♦ Reflex sympathetic dystrophy is characterized by intense prolonged pain, vasomotor disturbance, delayed functional recovery, and trophic changes♦ Avascular necrosis typically affects intra-articular bone after fracture and can occur in up to 70% of displaced talar neck fractures♦ Immobility associated with recovery from fracture is associated with deep vein thrombosis, which carries a risk of pulmonary embolism, and should be treated with anti-coagulants♦ Gas gangrene is a rapidly-spreading infection of devitalized tissue, removal of the affected area and treatment with penicillin is required♦ Compartment syndrome within a closed compartment can result in tissue ischaemia and necrosis followed by fibrosis and muscle contracture

35

Markus, Hugh, Anthony Pereira, and Geoffrey Cloud. Cerebral venous thrombosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198737889.003.0012.

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Most stroke results from arterial disease but venous occlusion can also cause stroke, and other neurological complications. This condition is uncommon and needs a high index of suspicion if it is not to be missed. The clinical presentations are varied and can mimic other neurological conditions. The diagnosis is important because with appropriate treatment the prognosis can be much better than for arterial infarction.

36

Wijdicks, Eelco F. M., and Sarah L. Clark. Drugs Used to Prevent Complications. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190684747.003.0017.

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Comprehensive neurosciences nursing care goes far in providing optimal support, but the acute immobilization and anticipated prolonged bed rest requires the use of prophylactic drugs. Many options relate to failure to move limbs, failure to breathe adequately and placement of intravenous catheters This chapter covers the more critical preventive measures.Prevention of deep venous thrombosis, hyperglycemia, stress ulcers, ventilator-associated pneumonia, urinary tract infections, vascular access infections, ventriculitis, and post-craniotomy infections are discussed in this chapter. Pharmacists assist in effective stewardship and surveillance of critically ill patients by helping select the appropriate antibiotics, determining the need for drug levels, and initiating or stopping preventative medications.

37

Huber, Kurt, and Joao Morais. Coagulation and thrombosis. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656653.003.0017.

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Antithrombotic therapy consisting of antiplatelet agents and/or anticoagulants is an important way to avoid atherothrombotic complications, especially in secondary prevention. Primary prevention by antithrombotic measures usually refers to the prevention of stroke in patients with atrial fibrillation and an increased risk for stroke or peripheral thromboembolic events by the use of anticoagulants. In certain situations a combination of anticoagulants and antiplatelet agents is mandatory. This chapter provides the pathophysiological background of coagulation and thrombosis, reports on the epidemiology of antithrombotic treatment, and describes the efficacy and safety of preventive antithrombotic measures in different cardiovascular indications. A short paragraph summarizes the current discussion of skipping aspirin in order to reduce the rate and severity of bleeding events.

38

Huber, Kurt, and Joao Morais. Coagulation and thrombosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199656653.003.0017_update_001.

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Antithrombotic therapy consisting of antiplatelet agents and/or anticoagulants is an important way to avoid atherothrombotic complications, especially in secondary prevention. Primary prevention by antithrombotic measures usually refers to the prevention of stroke in patients with atrial fibrillation and an increased risk for stroke or peripheral thromboembolic events by the use of anticoagulants. In certain situations a combination of anticoagulants and antiplatelet agents is mandatory. This chapter provides the pathophysiological background of coagulation and thrombosis, reports on the epidemiology of antithrombotic treatment, and describes the efficacy and safety of preventive antithrombotic measures in different cardiovascular indications. A short paragraph summarizes the current discussion of skipping aspirin in order to reduce the rate and severity of bleeding events.

39

Wiles, Kate, Kate Bramham, and Catherine Nelson-Piercy. Kidney disease. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198713333.003.0044.

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This chapter describes the physiological adaptations to pregnancy in women with and without renal disease, reports pregnancy outcomes in women with both acute kidney injury and chronic kidney disease, and discusses a management strategy for antenatal and peripartum care. Acute kidney injury (AKI) is difficult to define in pregnancy because of the physiological increase in glomerular filtration. A normal creatinine can mask renal injury in pregnancy. This chapter considers important causes of AKI in pregnancy including pre-eclampsia, HELLP syndrome, thrombotic microangiopathy, acute fatty liver of pregnancy, systemic lupus erythematosus, urinary tract infection, and obstruction. The trend in the developed world for delaying pregnancy and the increasing prevalence of obesity mean that greater numbers of pregnancies will be complicated by chronic kidney disease. Maternal and fetal complications increase with worsening prepregnancy renal function including the development of pre-eclampsia, fetal growth restriction, premature delivery, and fetal loss. Prepregnancy counselling and the intrapartum management for women with lupus nephritis, immunoglobulin A nephropathy, polycystic kidney disease, and diabetic nephropathy are discussed. Renal replacement therapies in pregnancy including both dialysis and renal transplantation are considered, and practical guidance on renal biopsy, anaesthesia, and the pharmacology of renal disease in pregnancy is offered.

40

Teoh, Eugene, and Michael J. Weston. Computed tomography. Edited by Christopher G. Winearls. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0014.

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Computed tomography (CT) has increased in use exponentially for the assessment of patients with renal tract pathology. This has been promoted by the availability of multidetector thin-slice CT so that intravenous urography has been superseded by CT urography. The latter may be considered as a ‘one-stop’ imaging investigation for haematuria, with increased detection of both urinary tract cancers and urolithiasis. Multiplanar reformats are made possible with the use of thin slices, allowing clear delineation of other pathologies such as urinary tract injury. In the transplant recipient, protocols have been developed for the assessment of more immediate complications such as thrombotic and stenotic disease. During follow-up, CT continues to inform the management of post-transplant lymphoproliferative disorder and other immunosuppressant-related complications. Unenhanced CT of the urinary tract has established its role in assessment of patients with renal colic, with the ability to detect pathology outside of the urinary tract. Renal CT has been developed for the characterization of renal masses, accompanied by the now well-established Bosniak renal cyst classification system. As the usefulness of CT increases, clear awareness of safety issues has to be maintained. These include the administration of intravenous iodinated contrast medium in higher-risk patient groups, particularly those with renal impairment. The radiation burden that comes with CT poses an added risk to the patient that should not be ignored. This necessitates clear referral guidelines for its use, which should be applied in careful balance with the global assessment of the patient.

41

Pichler, Michael R., and Robert D. Brown. Cerebral Venous Thrombosis. Edited by Emma Ciafaloni, Cheryl Bushnell, and Loralei L. Thornburg. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190667351.003.0017.

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Thrombosis of cortical veins and/or dural venous sinuses (CVT) is a rare but potentially devastating condition. CVT is more common in women and is strongly associated with pregnancy and the postpartum period, likely due to numerous procoagulant changes during this time. CVT can cause a wide range of symptoms depending on location of thrombosis. Clinical manifestations can include headache, cranial nerve deficits, seizures, and venous infarction with associated focal neurologic deficits. Severe cases may progress to coma and death, emphasizing the importance of early diagnosis and treatment. The approach to management of CVT during pregnancy and the postpartum period must be tailored to prevent complications to the mother and child. This chapter addresses the pathogenesis, clinical manifestations, diagnosis, and treatment of CVT in pregnancy and the postpartum period.

42

Paidas, Michael J., Nazli Hossain, Tahir S. Shamsi, Marc A. Rodger, and Jens Langhoff-Roos. Hemostasis and Thrombosis in Obstetrics and Gynecology. Wiley & Sons, Incorporated, John, 2011.

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43

Paidas, Michael J., Nazli Hossain, Tahir S. Shamsi, Marc A. Rodger, and Jens Langhoff-Roos. Hemostasis and Thrombosis in Obstetrics and Gynecology. Wiley & Sons, Limited, John, 2011.

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44

Paidas, Michael J., Nazli Hossain, Tahir S. Shamsi, Marc A. Rodger, and Jens Langhoff-Roos. Hemostasis and Thrombosis in Obstetrics and Gynecology. Wiley & Sons, Incorporated, John, 2011.

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45

Thrombosis in cardiovascular diseases. Philadelphia: Saunders, 1992.

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46

Moen, Vibeke. Neurological complications of neuraxial blockade. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198713333.003.0028.

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Neuraxial techniques for obstetric analgesia and anaesthesia are widespread, and serious complications are extremely rare. The most common of all complications following neuraxial blockade is postdural puncture headache, but headache may also be present in pathological conditions such as pre-eclampsia and sinus vein thrombosis. Headache may also be a symptom of cranial subdural haematoma, meningitis, and epidural abscess, all rare complications of central blockade, thus introducing a potential confounder in the newly delivered woman complaining of headache. Vertebral spinal haematomas are extremely rare in the healthy obstetric patient, but haemostatic disorders might develop following placement of an epidural catheter, thus increasing the possibility of spinal haematomas. Anaesthetists must be familiar with these rare complications, and perform neuraxial blockade avoiding traumatic damage, and using aseptic techniques. The anaesthetist will be involved in diagnosing a woman with neurological symptoms after labour and delivery, and must be familiar with common intrinsic obstetric neuropathies and clinical diagnostic procedures. This chapter describes complications following neuraxial blockade, as well as preventive and diagnostic procedures.

47

O'Brien, Patrick, and Hannah Cohen. Disorders of Thrombosis and Hemostasis in Pregnancy. Springer, 2012.

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48

Khorana, Alok A. Cancer-associated Thrombosis: New Findings in Translational Science, Prevention, and Treatment. Informa Healthcare, 2007.

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49

Paidas, Michael J., Nazli Hossain, Tahir S. Shamsi, Marc A. Rodger, and Jens Langhoff-Roos. Hemostasis and Thrombosis in Obstetrics and Gynecology. Wiley & Sons, Incorporated, John, 2010.

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50

Eisele, Ralf, and Lothar Kinzl. Thromboseprophylaxe in Unfallchirurgie und Orthopädie. Steinkopff-Verlag Darmstadt, 2007.

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