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1
Morganroth, Joel, and E. Neil Moore, eds. Risk/Benefit Analysis for the Use and Approval of Thrombolytic, Antiarrhythmic, and Hypolipidemic Agents. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-1605-3.
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2
Autar, Atmaram. Nursing assessment of clients at risk of deep vein thrombosis (DVT): Developing the Autar DVT scale. Birmingham: University of Central England in Birmingham, 1994.
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3
Autar, A. R. Advancing clinical practice in the management of Deep Vein Thrombosis (DVT): Development, application and evaluation of the Autar DVT risk assessment scale. Leicester: De Montfort University, 2002.
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4
Eric, Kasner Scott, and Gorelick Philip B, eds. Prevention and treatment of ischemic stroke. Philadelphia: Butterworth-Heinemann, 2004.
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5
Jørgen, Jespersen, Bertina Rogier M, Haverkate F. 1931-, European Concerted Action on Thrombosis and Disabilities (Committee), and Commission of the European Communities., eds. ECAT assay procedures: A manual of laboratory techniques. Dordrecht: Kluwer Academic Publishers, 1992.
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6
Joel, Morganroth, and Moore E. Neil, eds. Risk/benefit analysis for the use and approval of thrombolytic, antiarrhythmic, and hypolipidemic agents: Proceedings of the Ninth Annual Symposium on New Drugs & Devices, October 27 & 28, 1988. Boston: Kluwer Academic Publishers, 1989.
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7
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.
8
Alikhan, Raza. Prothrombotic conditions. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0285.
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The term thrombophilia is used to describe an individual who has a tendency to develop thrombosis. Arterial thrombosis is usually linked with classical risk factors such as age, smoking, hypertension, hyperlipidaemia, or diabetes; a thrombophilia assessment and workup is not usually considered in cases of arterial thrombosis. A clinically useful approach to the diagnosis and management of a patient with a venous thrombotic process is to categorize the disorder as either a primary (inherited) or secondary (acquired) hypercoagulable state. This topic addresses the diagnosis and management of prothrombotic conditions.
9
Provan, Drew, Trevor Baglin, Inderjeet Dokal, and Johannes de Vos. Haemostasis and thrombosis. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199683307.003.0010.
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Assessing haemostasis - The coagulation system - Laboratory tests - Platelets - Bleeding - Bleeding: laboratory investigations - Bleeding: therapeutic products - von Willebrand disease - Haemophilia A and B - Rare congenital coagulation disorders - Congenital thrombocytopenias - Congenital platelet function defects - Congenital vascular disorders - Haemorrhagic disease of the newborn - Thrombocytopenia (acquired) - Specific thrombocytopenic syndromes - Disseminated intravascular coagulation - Liver disease - Renal disease - Acquired anticoagulants and inhibitors - Treatment of spontaneous FVIII inhibitor - Acquired disorders of platelet function - Henoch–Schönlein purpura - Perioperative bleeding and massive blood loss - Massive blood loss - Heparin - Heparin induced thrombocytopenia/with thrombosis (HIT/T) - Oral anticoagulant therapy (warfarin, VKAs) - New oral anticoagulant drugs - Thrombosis - Risk assessment and thromboprophylaxis - Example of VTE risk assessment - Heritable thrombophilia - Acquired thrombophilia - Thrombotic thrombocytopenic purpura (TTP) - Haemolytic uraemic syndrome (HUS) - Heparin-induced thrombocytopenia (HIT)
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Provan, Drew, Trevor Baglin, Inderjeet Dokal, Johannes de Vos, and Angela Theodoulou. Haemostasis and thrombosis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199683307.003.0010_update_001.
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Assessing haemostasis - The coagulation system - Laboratory tests - Platelets - Bleeding - Bleeding: laboratory investigations - Bleeding: therapeutic products - von Willebrand disease - Haemophilia A and B - Rare congenital coagulation disorders - Congenital thrombocytopenias - Congenital platelet function defects - Congenital vascular disorders - Haemorrhagic disease of the newborn - Thrombocytopenia (acquired) - Specific thrombocytopenic syndromes - Disseminated intravascular coagulation - Liver disease - Renal disease - Acquired anticoagulants and inhibitors - Treatment of spontaneous FVIII inhibitor - Acquired disorders of platelet function - Henoch–Schönlein purpura - Perioperative bleeding and massive blood loss - Massive blood loss - Heparin - Heparin induced thrombocytopenia/with thrombosis (HIT/T) - Oral anticoagulant therapy (warfarin, VKAs) - New oral anticoagulant drugs - Thrombosis - Risk assessment and thromboprophylaxis - Example of VTE risk assessment - Heritable thrombophilia - Acquired thrombophilia - Thrombotic thrombocytopenic purpura (TTP) - Haemolytic uraemic syndrome (HUS) - Heparin-induced thrombocytopenia (HIT)
11
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.
12
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.
13
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.
14
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.
15
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.
16
Singer, Mervyn. Pathophysiology and causes of pulmonary embolism. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0170.
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Pulmonary embolus is predominantly due to thrombus breaking off from deep veins or from within the right heart, lodging within large or small vessels within the pulmonary vasculature, causing a variable degree of clinical features ranging from asymptomatic through to shock and cardiac arrest. Non-thrombotic causes include air or fat embolism. Outcome is predicated by the degree of right ventricular dysfunction. There are multiple risk factors including surgery, arrhythmias, prolonged immobility, venous stasis, pregnancy and an underlying pro-thrombotic tendency, either congenital or acquired. Numerous risk stratification scores have been developed derived from clinical features, imaging findings and biochemical markers of right ventricular strain and myocardial damage.
17
Shrivastava, Seema, Beverley J. Hunt, and Anthony Dorling. Coagulopathies in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0135.
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Coagulation abnormalities are common in chronic kidney disease (CKD). Both haemorrhage and thrombosis are more common than in the general population. Haemorrhage, when it occurs, is associated with increased morbidity and mortality compared to that seen in non-uraemic patients. It is more likely spontaneously, but particularly in association with anti-platelet agents or anticoagulants. The increased risk of both arterial and venous thrombosis occurs in part because of the increase prevalence of traditional risk factors for thrombosis in CKD, in part because of the specific problems associated with nephrotic syndrome, and also because of specific putative prothrombotic factors associated with CKD, such as increased levels of coagulation factors and altered platelet function associated with uraemia. Two syndromes, both characterized by intravascular thrombosis can contribute to the development of CKD. The first is antiphospholipid syndrome, due to the presence of antibodies against negatively charged phospholipids, in which thrombosis of the renal vasculature is relatively common. The second is a group of conditions, the thrombotic microangiopathies, in which inherited or acquired deficiencies of ADAMTS13, antiphospholipid antibodies, or pathological endothelial cell activation in renal vessels, sometimes due to functional deficiencies of one or more proteins regulating coagulation or complement activation, leads to acute renal dysfunction associated with anaemia.
18
Balik, Martin. Perioperative cardiac care of the high-risk non-cardiac patient. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0076.
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Non-cardiac surgery conveys a cardiac risk related to the status of the patient’s cardiovascular system. Cardiac-related risk of surgery can be assessed by integrating the risk and urgency of the procedure with cardiovascular risk factors, which include age, ischaemic heart disease, heart failure, stroke, diabetes mellitus, chronic obstructive pulmonary disease, and renal dysfunction. An individual assessment can include simple multivariate scoring systems, developed with the aim of evaluating cardiac risk prior to non-cardiac surgery. Patient assessment can be extended for indicated additional tests. The indications for further cardiac testing and treatments are the same as in the non-operative setting, but their timing is dependent on the urgency of surgery, and patient-specific and surgical risk factors. A delay in surgery, due to the use of both non-invasive and invasive preoperative testing, should be limited to those circumstances in which the results of such tests will clearly affect patient management. In high-risk patients, the result of the cardiac assessment helps to choose adequate perioperative monitoring and to indicate for an intensive care unit stay perioperatively. Chronic medications can be adjusted, according to the current knowledge on perioperative management. Drugs with the potential to reduce the incidence of post-operative cardiac events and mortality include beta-blockers, statins, and aspirin. Chronic platelet anti-aggregation and anticoagulation therapies have to be adapted by weighing the risk of bleeding against the risk of thrombotic complications.
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Balik, Martin. Perioperative cardiac care of the high-risk non-cardiac patient. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199687039.003.0076_update_001.
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Non-cardiac surgery conveys a cardiac risk related to the status of the patient’s cardiovascular system. Cardiac-related risk of surgery can be assessed by integrating the risk and urgency of the procedure with cardiovascular risk factors, which include age, ischaemic heart disease, heart failure, stroke, diabetes mellitus, chronic obstructive pulmonary disease, and renal dysfunction. An individual assessment can include simple multivariate scoring systems, developed with the aim of evaluating cardiac risk prior to non-cardiac surgery. Patient assessment can be extended for indicated additional tests. The indications for further cardiac testing and treatments are the same as in the non-operative setting, but their timing is dependent on the urgency of surgery, and patient-specific and surgical risk factors. A delay in surgery, due to the use of both non-invasive and invasive preoperative testing, should be limited to those circumstances in which the results of such tests will clearly affect patient management. In high-risk patients, the result of the cardiac assessment helps to choose adequate perioperative monitoring and to indicate for an intensive care unit stay perioperatively. Chronic medications can be adjusted, according to the current knowledge on perioperative management. Drugs with the potential to reduce the incidence of post-operative cardiac events and mortality include beta-blockers, statins, and aspirin. Chronic platelet anti-aggregation and anticoagulation therapies have to be adapted by weighing the risk of bleeding against the risk of thrombotic complications.
20
Balik, Martin. Perioperative cardiac care of the high-risk non-cardiac patient. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0076_update_002.
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Non-cardiac surgery conveys a cardiac risk related to the status of the patient’s cardiovascular system. Cardiac-related risk of surgery can be assessed by integrating the risk and urgency of the procedure with cardiovascular risk factors, which include age, ischaemic heart disease, heart failure, stroke, diabetes mellitus, chronic obstructive pulmonary disease, and renal dysfunction. An individual assessment can include simple multivariate scoring systems, developed with the aim of evaluating cardiac risk prior to non-cardiac surgery. Patient assessment can be extended for indicated additional tests. The indications for further cardiac testing and treatments are the same as in the non-operative setting, but their timing is dependent on the urgency of surgery, and patient-specific and surgical risk factors. A delay in surgery, due to the use of both non-invasive and invasive preoperative testing, should be limited to those circumstances in which the results of such tests will clearly affect patient management. In high-risk patients, the result of the cardiac assessment helps to choose adequate perioperative monitoring and to indicate for an intensive care unit stay perioperatively. Chronic medications can be adjusted, according to the current knowledge on perioperative management. Drugs with the potential to reduce the incidence of post-operative cardiac events and mortality include beta-blockers, statins, and aspirin. Chronic platelet anti-aggregation and anticoagulation therapies have to be adapted by weighing the risk of bleeding against the risk of thrombotic complications.
21
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.
22
Stanworth, Simon, and Stuart McKechnie. Pathophysiology of disordered coagulation. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0269.
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Imbalances in the regulation of haemostasis may manifest as bleeding (depletion of pro-coagulant factors) or thrombosis (deficiency of anti-coagulants). Disordered haemostasis is common in critically-ill patients and may result from infection, trauma, haemorrhage, inflammation, organ dysfunction (notably renal and liver dysfunction), or drug therapy. Complex patterns of coagulopathy where both bleeding and prothrombotic tendencies co-exist are well recognized in critical illness. The limitations of standard laboratory coagulation tests to predict bleeding risk, including activated partial thromboplastin time and prothrombin time, are well recognized. These assays were developed for diagnosis of inherited bleeding disorders or for monitoring of anticoagulant therapy. This has led to increased interest in global haemostatic tests, such as viscoelastic and thrombin generation tests. Thromboembolism is an important cause of morbidity and mortality in critically-ill patients. While inherited causes of bleeding appear to be often related to single gene abnormalities, thrombotic tendencies appear to reflect more complex interactions between inherited and acquired factors. Many interactions exist between coagulation pathways and inflammation. Systemic inflammation triggers widespread activation of coagulation, with pro-inflammatory cytokines activating pro-coagulant pathways and downregulating anticoagulant pathways. A net result of this interaction between inflammatory and coagulation pathways in sepsis is thrombin generation, intravascular fibrin deposition and a consumptive coagulopathy.
23
Visser, Frans, and Maarten Simoons. Percutaneous Coronary Intervention and Thrombolysis in AMI & other ACS. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199544769.003.0003.
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• Acute coronary syndromes (ACS) comprise an evolving acute myocardial infarction (AMI) presenting with or without ST-elevation and unstable angina• Patients presenting with an ST-elevation MI require immediate reperfusion therapy by primary percutaneous coronary intervention (PCI) or, if such is not available, thrombolysis• Cardiologists, emergency care physicians, general practictioners and ambulance services should collaborate to develop a national or regional system to optimise AMI therapy, given the national or local facilities and available resources• A subgroup of high-risk patients presenting with ACS without ST-elevation benefit from PCI or coronary artery bypass graft surgery• In all patients with ACS intensive anti-platelet and anti-thrombotic therapy is warranted, as well as B-blockers, ACE-inhibitors and statins.
24
Whitworth, Caroline, and Stewart Fleming. Malignant hypertension. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0216.
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Malignant hypertension (MH) is recognized clinically by elevated blood pressure together with retinal haemorrhages or exudates with or without papilloedema (grades III or IV hypertensive retinopathy); and may constitute a hypertensive emergency or crisis when complicated by evidence of end-organ damage including microangiopathic haemolysis, encephalopathy, left ventricular failure, and renal failure. Though reversible, it remains a significant cause of end-stage renal failure, and of cardiovascular and cerebrovascular morbidity and mortality in developing countries.MH can complicate pre-existing hypertension arising from diverse aetiologies, but most commonly develops from essential hypertension. The absolute level of blood pressure appears not to be critical to the development of MH, but the rate of rise of blood pressure may well be relevant in the pathogenesis. The pathogenesis of this transformation remains unclear.The pathological hallmark of MH is the presence of fibrinoid necrosis (medial vascular smooth muscle cell necrosis and fibrin deposition within the intima) involving the resistance arterioles in many organs. Fibrinoid necrosis is not specific to MH and this appearance is seen in other conditions causing a thrombotic microangiopathy such as haemolytic uraemic syndrome, scleroderma renal crisis, antiphospholipid syndrome, and acute vascular rejection post transplant. MH can both cause a thrombotic microangiopathy (TMA) but can also complicate underlying conditions associated with TMA.The pathophysiological factors that interact to generate and sustain this condition remain poorly understood. Risk factors include Afro-Caribbean race, smoking history, younger age of onset of hypertension, previous pregnancy, and untreated hypertension associated with non-compliance or cessation of antihypertensive therapy.Evidence from clinical studies and animal models point to a central role for the intrarenal renin–angiotensin system (RAS) in MH; there is good evidence for renal vasoconstriction and activation of the renal paracrine RAS potentiating MH once established; however, there may also be a role in the predisposition of MH suggested by presence of increased risk conferred by an ACE gene polymorphism in humans and polymorphisms for both ACE and AT1 receptor in an animal model of spontaneous MH. Other vasoactive mediators such as the endothelin and the inflammatory response may be important contributing to and increasing endothelial damage. There have been no randomized controlled trials to define the best treatment approach, but progressive lowering of pressures over days is considered safest unless made more urgent by critical clinical state. It seems logical to introduce ACE inhibition cautiously and early, but in view of the risk of rapid pressure lowering some recommend delay.
25
Kothari, Jaimal, and Marie Scully. Thrombocytopenia in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0272.
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Thrombocytopenia is an extremely common finding in patients in intensive care. This can lead to serious morbidity and mortality from bleeding, and also uncertainty with regards to how to assess this risk in the wider context of the underlying pathology, which may be multifactorial, when specific blood products should be transfused, and the associated risks of carrying out interventional procedures. Haemodilution, platelet consumption, increased platelet destruction, reduced production, and increased sequestration are the main mechanisms that account for thrombocytopenia, and in the ICU setting there is typically an interplay of more than one of these that accounts for the counts seen. Sepsis and disseminated intravascular coagulation are the most common causes of thrombocytopenia in the ICU, with significant overlap between the pathologies. Less common causes in an intensive care unit setting include heparin-induced thrombocytopenia (HIT) and thrombotic thromobocytopenic purpura (TTP). The evidence base surrounding platelet thresholds remains poor and is an active area of research. Anticoagulation in the context of thrombocytopenia is problematic and requires a patient-specific approach.
26
Venous Thrombosis: Risk Factors, Management and Complications. Nova Science Pub Inc, 2014.
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27
Deep Vein Thrombosis (Key Management Skills in Nursing). Quay Books,a division of Mark Allen Publishing Ltd, 1996.
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28
Kahn, S. Lowell. Directional AngioJet Thrombectomy with Guide Catheter Helical Spin Technique. Edited by S. Lowell Kahn, Bulent Arslan, and Abdulrahman Masrani. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199986071.003.0037.
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The presence of thrombus in the central veins is associated with a higher risk of development post-thrombotic syndrome. The AngioJet Solent Proxi (90 cm) and Omni (120 cm) catheters are commonly used peripheral thrombectomy devices indicated for acute arterial and venous thrombus removal. Both catheters are 6 Fr sheath/8 Fr guide catheter compatible, and both offer the Power Pulse feature, allowing the direct infusion of tissue plasminogen activator into the thrombus. The catheters are indicated for use in vessels greater than 3 mm, with an optimal vessel range between 6 and 20 mm. Their use in the removal of iliac vein and inferior vena cava thrombus is frequent. Although the system is purported to provide effective thrombectomy capabilities in larger vessels, incomplete thrombus removal is common with larger vessels. This chapter proposes a simple modification in the standard use of the AngioJet Solent Proxi and Omni catheters.
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Deep-Vein Thrombosis: Risk Factors, Treatment and Clinical Outcomes. Nova Science Pub Inc, 2014.
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30
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.
31
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.
32
Warwick, David. Prevention of thrombosis in orthopaedic surgery. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199550647.003.0006.
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♦ The risk–benefit of thromboprophylaxis in orthopaedic surgery remains unclear♦ Some conditions, such as major trauma, carry a much higher risk than others, such as routine knee replacement♦ Some patients appear to be genetically more predisposed than others♦ In trials of efficacy of thromboembolism, the use of deep vein thrombosis as a surrogate endpoint for death from a pulmonary embolus may not be completely reliable♦ There is a variety of mechanical and chemical methods available, each of which has real and potential advantages as well as real and potential dangers♦ Even the length of time that a patient is at risk after major surgery is unclear♦ Clinicians should adhere to guidelines where possible.
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Wiles, Kate, and Catherine Nelson-Piercy. Contraception in patients with kidney disease. Edited by Norbert Lameire and Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0293_update_001.
Full textAbstract:
Three per cent of women of childbearing age have chronic kidney disease, and although end-stage renal failure impacts on fertility, conception and high-risk pregnancy do occur. Following renal transplantation, the patient should understand the potential impact of a pregnancy on transplant function and vice versa. Surveys show that a large proportion of pregnancies in female renal patients are unplanned. The effectiveness of a particular contraceptive method is dependent upon acceptability to the patient and compliance. Contraceptive decision-making needs to balance acceptability and safety with the risk of an unplanned pregnancy. Oestrogen-containing contraceptive methods are considered unacceptable for many renal patients because of their association with increased blood pressure and thrombotic and vascular events. Progesterone-only methods have an advantageous safety profile. The progesterone-only pill (desogestrel preparations), intrauterine system (Mirena®), and implant (Nexplanon®) are safe and effective in women with CKD. Concerns regarding the intrauterine system (Mirena®) in women taking immunosuppression are unfounded and observational evidence does not demonstrate an increased risk of infection. Sterilization is effective and should be considered to be irreversible. The effectiveness of barrier methods is reduced when ‘typical use’ is compared to ‘perfect use’. Unplanned pregnancy rates are high with fertility awareness methods and reliance on lactational amenorrhoea is not advocated.Interactions between drugs which are commonly prescribed in the renal population and different contraceptive methods are outlined in this chapter.
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Hvas, Anne-Mette, Erik L. Grove, and Steen Dalby Kristensen. Biomarkers of coagulation and thrombosis. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0038.
Full textAbstract:
Coagulation is evaluated by conventional coagulation analyses, often supplemented by point-of-care tests. Recently, a number of point-of-care tests for evaluation of platelet function and the efficacy of antiplatelet therapy has been investigated. Thrombophilia contributes to the risk of thrombosis, and a battery of complex assays is required to identify all thrombophilias. Disseminated intravascular coagulation is characterized by microthrombosis and clinical bleeding. A scoring system for overt disseminated intravascular coagulation provides a five-step diagnostic algorithm. The cornerstone of the management of disseminated intravascular coagulation is treatment of the underlying triggering condition. Heparin-induced thrombocytopenia is an adverse immunological effect of heparin therapy. Besides thrombocytopenia, the major clinical consequence of heparin-induced thrombocytopenia is an increased risk of thrombosis. The diagnosis is based on clinical symptoms and detection of platelet-activating heparin-induced thrombocytopenia antibodies. When heparin-induced thrombocytopenia is strongly suspected, it is recommended to stop heparin treatment, investigate for heparin-induced thrombocytopenia antibodies, and initiate non-heparin anticoagulant treatment.
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Hvas, Anne-Mette, Erik L. Grove, and Steen Dalby Kristensen. Biomarkers of coagulation and thrombosis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0038_update_001.
Full textAbstract:
Coagulation is evaluated by conventional coagulation analyses, often supplemented by point-of-care tests. Recently, a number of point-of-care tests for evaluation of platelet function and the efficacy of antiplatelet therapy has been investigated. Thrombophilia contributes to the risk of thrombosis, and a battery of complex assays is required to identify all thrombophilias. Disseminated intravascular coagulation is characterized by microthrombosis and clinical bleeding. A scoring system for overt disseminated intravascular coagulation provides a five-step diagnostic algorithm. The cornerstone of the management of disseminated intravascular coagulation is treatment of the underlying triggering condition. Heparin-induced thrombocytopenia is an adverse immunological effect of heparin therapy. Besides thrombocytopenia, the major clinical consequence of heparin-induced thrombocytopenia is an increased risk of thrombosis. The diagnosis is based on clinical symptoms and detection of platelet-activating heparin-induced thrombocytopenia antibodies. When heparin-induced thrombocytopenia is strongly suspected, it is recommended to stop heparin treatment, investigate for heparin-induced thrombocytopenia antibodies, and initiate non-heparin anticoagulant treatment.
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Pruthi, Rajiv K. Coagulation (Hemostasis and Thrombosis). Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0295.
Full textAbstract:
The coagulation system has 2 essential functions: to maintain hemostasis and to prevent and limit thrombosis. The procoagulant component of the hemostatic system prevents and controls hemorrhage. Vascular injury results in activation of hemostasis, which consists of vasospasm, platelet plug formation (platelet activation, adhesion, and aggregation), and fibrin clot formation (by activation of coagulation factors in the procoagulant system). The anticoagulant system prevents excessive formation of blood clots, and the fibrinolytic system breaks down and remodels blood clots. Quantitative abnormalities (deficiencies) and qualitative abnormalities of platelets and coagulation factors lead to bleeding disorders, whereas deficiencies of the anticoagulant system are risk factors for thrombosis. Common disorders of hemostasis and thrombosis are reviewed.
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Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0040.
Full textAbstract:
Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the extracellular matrix and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated monocytes differentiate into macrophages which acquire a specialized phenotypic polarization (protective or harmful), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoprotein via low-density lipoprotein receptor-related protein-1 receptors. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Both lipid-laden vascular smooth muscle cells and macrophages release the procoagulant tissue factor, contributing to thrombus propagation. Platelets also participate in progenitor cell recruitment and drive the inflammatory response mediating the atherosclerosis progression. Recent data attribute to microparticles a potential modulatory effect in the overall atherothrombotic process. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be modulated.
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Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0040_update_001.
Full textAbstract:
Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the intimal layer and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles attached to the extracellular matrix suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated pro-atherogenic monocytes (mainly Mon2) differentiate into macrophages which acquire a specialized phenotypic polarization (protective/M1 or harmful/M2), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoproteins via low-density lipoprotein receptor-related protein-1 receptors becoming foam cells. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels and calcium deposits increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces rich in tissue factor that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Platelets also participate in leucocyte and progenitor cell recruitment are likely to mediate atherosclerosis progression. Recent data attribute to microparticles a modulatory effect in the overall atherothrombotic process and evidence their potential use as systemic biomarkers of thrombus growth. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be prevented and modulated.
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Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0040_update_002.
Full textAbstract:
Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the intimal layer and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles attached to the extracellular matrix suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated pro-atherogenic monocytes (mainly Mon2) differentiate into macrophages which acquire a specialized phenotypic polarization (protective/M1 or harmful/M2), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoproteins via low-density lipoprotein receptor-related protein-1 receptors becoming foam cells. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels and calcium deposits increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces rich in tissue factor that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Platelets also participate in leucocyte and progenitor cell recruitment are likely to mediate atherosclerosis progression. Recent data attribute to microparticles a modulatory effect in the overall atherothrombotic process and evidence their potential use as systemic biomarkers of thrombus growth. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be prevented and modulated.
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Dawson, Dana, and Keith Fox. Anti-Platelet and Anti-Thrombotic Therapy Post-AMI. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199544769.003.0004.
Full textAbstract:
• Acute coronary syndromes (ACS) encompass a spectrum of presentations which include unstable angina, non-ST-elevation myocardial infarction (NSTEMI or NSTE-ACS), and ST-elevation myocardial infarction (STEMI or STE-ACS)• Anti-platelet and anti-thrombotic agents are administered as ancillary therapy to myocardial reperfusion in patients presenting with an acute coronary syndrome, to maintain the patency of the infarct-related coronary artery• More specific and potent inhibitors of platelet activation and of the coagulation cascade are emerging with the aim being to further improve clinical outcomes in patients presenting with an acute coronary syndrome, without increasing the risks of major bleeding.
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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.
Full textAbstract:
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.
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Chan, Chee M., and Andrew F. Shorr. Prevention and management of thrombosis in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0271.
Full textAbstract:
Venous thromboembolism (VTE) represents a significant challenge in the care of critically-ill patients. Because of a combination of factors including comorbidities, their acute illness, and medical interventions, patients in the intensive care unit (ICU) face a heightened risk for VTE. In addition, because of their impaired physiological reserves, critically-ill subjects will not tolerate events, such as pulmonary emboli (PEs), well. A number of recent studies better describe the epidemiology and outcomes related to VTE acquired in the ICU. New research also explores optimal approaches for VTE prevention and better defines the risk for bleeding associated with pharmacological preventive options. This chapter reviews the epidemiology of, outcomes related to, and preventive strategies for VTE in the ICU. It also discusses diagnostic options in addition to focusing on selected populations at very high risk for VTE in the ICU, namely trauma patients and those who have suffered a stroke.
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Morganroth, J. "Risk/Benefit Analysis for the Use and Approval of Thrombolytic, Antiarrhythmic, and Hypolipidemic Agents". Springer, 2011.
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Khouri, George, Shelly Ozark, and Bruce Ovbiagele. Common Risk factors for Stroke and Medical Prevention Therapies. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0103.
Full textAbstract:
Stroke from thrombosis or emboli in cerebral vessels or hemorrhage is one of the most commonly encountered and most devastating neurological diseases. Rapid loss of function occurs due to an interruption of blood supply to the brain, leading to tissue ischemia and cell death. The risk of both ischemic and hemorrhagic stroke doubles for each successive decade after age 55, which is likely independent of other risk factors such as diabetes, hypertension, and hyperlipidemia. Lifestyle modifications, antiplatelet therapy and control of hyperlipidemia and hypertension are the mainstays of prevention.
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Zhu, Nancy Y., and Cynthia Wu. Anaemia, cytopenias, and thrombosis in palliative medicine. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656097.003.0083.
Full textAbstract:
Many haematological issues can complicate end-of-life care, including cytopenias and venous thromboembolism (VTE). Anaemia is very common and can significantly impact quality of life; causes include haemorrhage, iron deficiency, nutritional deficiencies, and bone marrow infiltration. Neutropenia from bone marrow failure as a result of disease infiltration or from chemotherapy effects can result in life-threatening infections. Finally, VTE is commonly seen in cancer patients as well as those who require prolonged hospitalization. Symptoms can cause discomfort, mortality is increased, and treatment is associated with major bleeding. Understanding the therapeutic options and their adverse side effects is essential in the management of these complex problems. Despite the presence of effective therapies, it is also important to realize that events such as febrile neutropenia and pulmonary embolism are often seen at the end of life and intervention may not always impact prognosis. The risks of intervention should be weighed against expected benefits when developing appropriate palliative care plans.
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Khorana, Alok A., and Charles W. Francis. Cancer-Associated Thrombosis: New Findings in Translational Science, Prevention, and Treatment. Taylor & Francis Group, 2007.
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Khorana, Alok A., and Charles W. Francis. Cancer-Associated Thrombosis: New Findings in Translational Science, Prevention, and Treatment. Taylor & Francis Group, 2007.
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(Editor), Alok A. Khorana, and Charles W. Francis (Editor), eds. Cancer-Associated Thrombosis: New Findings in Translational Science, Prevention, and Treatment. Informa Healthcare, 2007.
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Kahn, S. Lowell. Balloon-Assisted Removal of the Trapped Catheter. Edited by S. Lowell Kahn, Bulent Arslan, and Abdulrahman Masrani. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199986071.003.0048.
Full textAbstract:
Although uncommon, a trapped central venous catheter (CVC) can present a significant problem for the interventionalist and pose considerable risk to the patient. The use of chronic long-term CVCs is on the rise, with an average catheter dwell time of 10 months. Although all CVCs are prone to complications, chronic catheters exhibit a higher rate of complications. Chronic catheters are also at risk of becoming trapped, whereby they cannot be removed by standard technique. A simple, elegant technique to remove a trapped CVC via inserting an angioplasty balloon into the lumen of a stuck catheter has been described, as has a modified technique with inclusion of a hemostatic sheath and a stiff guidewire inserted into the cut catheter to ensure hemostasis, prevent air embolism or endoluminal thrombosis, and avoid injury to the central veins and heart. Examples of both applications are provided in this chapter.
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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.