Książki na temat „Ischaemia-reperfusion”
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1
A, Grace P., i Mathie Robert T, red. Ischaemia reperfusion injury. Oxford: Blackwell Science, 1999.
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2
Khaira, Harmeet Singh. Ischaemia-reperfusion in intermittent claudication. Birmingham: University of Birmingham, 1995.
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3
Wilson, Ian Clark. The role of leucocytes in neonatal myocardial ischaemia-reperfusion injury. Birmingham: University of Birmingham, 1994.
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4
Herman, Stanley Leon. Age differences in the susceptibility of the normal rabbit myocardium to injury following ischaemia and reperfusion. Ottawa: National Library of Canada, 1992.
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5
Alfred Benzon Symposium (41st 1996 Royal Danish Academy of Sciences and Letters). Coronary microcirculation during ischaemia and reperfusion: Proceedings of a symposium held at the Royal Danish Academy of Sciences and Letters, August 18-22, 1996. Redaktorzy Aldershvile Jan, Haunsø Stig i Svendsen Jesper Hastrup. Copenhagen: Munksgaard, 1997.
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6
Haunso. Coronary Microcirculation During Ischaemia & Reperfusion. Blackwell Science Inc, 1997.
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7
Fink, Mitchell P. Ischaemia-reperfusion injury in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0308.
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Ischaemia/reperfusion (I/R) injury contributes to the pathogenesis of many common clinical conditions, including stroke, myocardial damage after percutaneous intervention for acute coronary artery occlusion, primary graft dysfunction after solid organ transplantation. The mechanisms that are responsible for I/R injury remain incompletely understood, but damage caused by reactive oxygen species (ROS) and reactive nitrogen species clearly is important. A number of therapeutic approaches, such as administration of ROS scavengers, are effective in animal models of I/R injury, but for the most part, translation of these findings into strategies that can clearly benefit patients has yet to be achieved.
8
Hausenloy, Derek, i Derek Yellon, red. An Introduction to Cardioprotection. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199544769.003.0001.
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• In its broadest sense, the term ‘cardioprotection’ encompasses ‘all mechanisms and means that contribute to the preservation of the heart by reducing or even preventing myocardial damage’• However, for the purposes of this book, the term ‘cardioprotection’ will refer to the endogenous mechanisms and therapeutic strategies that reduce or prevent myocardial damage induced by acute ischaemia-reperfusion injury• In this context, cardioprotection begins with the primary prevention of coronary heart disease and includes the reduction of myocardial injury sustained during coronary artery bypass graft surgery, and an acute myocardial infarction, conditions with considerable morbidity and mortality• An understanding of the pathophysiology of acute myocardial ischaemia-reperfusion injury is essential when designing new cardioprotective strategies• Several methods exist for both quantifying myocardial damage induced by acute ischaemia-reperfusion injury and for assessing myocardial salvage following the application of cardioprotective strategies• Importantly, novel cardioprotective strategies must be capable of preventing and reducing myocardial damage over and above that provided by current optimal therapy.
9
Downey, James, i Michael Cohen. Endogenous Mechanisms of Cardioprotection. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199544769.003.0008.
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• Ischaemic preconditioning is the most powerful endogenous mechanism for limiting myocardial infarct size in the experimental setting. Its clinical application is limited to scenarios in which the index episode of ischaemia and reperfusion can be anticipated such as in the setting of cardiac surgery• Ischaemic postconditioning represents an endogenous cardioprotective strategy which is applied at the onset of myocardial reperfusion, thereby allowing its use as an adjunct to reperfusion in patients presenting with an acute myocardial infarction• Both ischaemic preconditioning and postconditioning recruit a common signal transduction pathway at the time of myocardial reperfusion, which can be targeted by pharmacological agents administered as adjuncts to reperfusion.
10
Jumean, Marwan F., i Mark S. Link. Post-cardiac arrest arrhythmias. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0065.
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Our understanding of arrhythmias following resuscitated cardiac arrest has evolved over the past two decades to entail complex pathophysiological processes including, in part, ischaemia and ischaemia-reperfusion injury. Electrical instability after the return of spontaneous circulation (ROSC) is common, ranging from atrial fibrillation to recurrent ventricular tachycardia and fibrillation. Electrical instability following out-of-hospital cardiac arrest is most commonly due to myocardial ischaemia and post-arrest myocardial dysfunction. However, electrolyte disturbances, elevated catecholamine levels, the frequent use of vasopressors and inotropes, and underlying structural heart disease or channelopathies also contribute in the acute setting. Limited data exists that specifically address the management of arrhythmias in the immediate post-arrest period. In addition to treating any potential reversible cause, the management in the haemodynamically-stable patient includes beta-blockers, class I (lignocaine and procainamide) and III anti-arrhythmic agents (amiodarone). Defibrillation is often needed for recurrent ventricular arrhythmias.
11
Nolan, Jerry P., i Michael J. A. Parr. Management after resuscitation from cardiac arrest. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0066.
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Systemic ischaemia during cardiac arrest and the reperfusion response after return of spontaneous circulation (ROSC) cause the post-cardiac arrest syndrome (PCAS). The severity and duration of this syndrome is determined by the cause and duration of cardiac arrest, quality of resuscitation, and interventions after ROSC. Four key clinical components are recognized—post-cardiac arrest brain injury, myocardial dysfunction, other organ ischaemia/reperfusion (e.g. liver, kidney), and potential persistence of the precipitating pathology causing the cardiac arrest. The interventions applied after ROSC impact significantly on the quality of survival. All components of the PCAS need to be addressed if outcome is to be optimized; treatment should start immediately after ROSC. An ‘ABCDE’ (Airway, Breathing, Circulation, Disability, Exposure) systems approach is used to identify and treat physiological abnormalities and organ injury. All survivors of out-of-hospital cardiac arrest should be considered for urgent coronary angiography unless the cause of cardiac arrest is clearly non-cardiac or continued treatment is considered futile. Targeted temperature management (mild hypothermia and avoidance of hyperthermia) should be considered for those patients who remain comatose after ROSC. If targeted temperature management has been used, early prognostication on outcome is unreliable and should be delayed until 3 days after return to normothermia; it should not rely on just one modality.
12
Ramsay, Michael A. E. Anaesthesia for transplant surgery. Redaktor Philip M. Hopkins. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0067.
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The provision of anaesthesia for organ transplantation requires a team of specialist anaesthetists who are available 24 hours a day. The cold and warm ischaemia times may have very deleterious effects on the graft. The team must have a basic understanding of the immune system and the strategies of immunosuppression therapy. The preoperative assessment of the patient requires an understanding of the cause and effects of the compromised organ that is to be replaced. The procedure in many instances will result in a reperfusion syndrome when the graft is revascularized and also an ischaemia–reperfusion injury. The understanding of these entities is essential as is the preparation and protocols to treat or ameliorate the effects of these syndromes if they occur. The preparation for many organ transplants includes invasive monitoring of haemodynamics, cardiac function, pulmonary function, and acid–base balance. Access for massive transfusion therapy and coagulation assessment is essential for many transplant procedures. The maintenance of body temperature and fluid balance may be challenging. The protection and monitoring of the function of major organs such as the brain, heart, lungs, and kidneys is essential but the homeostasis of endocrine function and electrolytes is also important. The provision of excellent anaesthesia is a key component of a successful transplant programme. A small team of highly trained professionals with extensive training and experience in transplant anaesthesia provide the best results.
13
López-Sendón, José, i Esteban López de Sá. Mechanical complications of myocardial infarction. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0045.
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Mechanical complications after an acute infarction include different forms of heart rupture, including free wall rupture, interventricular septal rupture, and papillary muscle rupture. Its incidence decreased dramatically with the widespread use of reperfusion therapies but may occur in 2–3% of ST-elevation myocardial infarction patients, and mortality is very high if not properly diagnosed, as surgery is the only effective treatment. Echocardiography is the most important tool for diagnosis that should be suspected in patients with hypotension, heart failure, or recurrent chest pain. Awareness and well-established protocols are crucial for an early diagnosis. Modern imaging techniques permit a more reliable and direct identification of left ventricular free wall rupture, which is almost impossible to identify with conventional echocardiography. Mitral regurgitation, secondary to papillary muscle ischaemia or necrosis or left ventricular dilatation and remodelling, without papillary muscle rupture, is frequent after myocardial infarction and is considered as an independent risk factor for outcomes. Revascularization to control ischaemia and surgical repair should be considered in all patients with severe or symptomatic mitral regurgitation in the absence of severe left ventricular dysfunction. Other mechanical complications include true aneurysms and thrombus formation in the left ventricle. Again, these complications have decreased with the use of early reperfusion therapies and, for thrombus formation, with aggressive antithrombotic treatment. In a single large randomized trial (STICH), surgical remodelling of the left ventricle failed to demonstrate a significant improvement in outcomes, although it still may be an option in selected patients.
14
López-Sendón, José, i Esteban López de Sá. Mechanical complications of myocardial infarction. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199687039.003.0045_update_001.
Pełny tekst źródłaStreszczenie:
Mechanical complications after an acute infarction include different forms of heart rupture, including free wall rupture, interventricular septal rupture, and papillary muscle rupture. Its incidence decreased dramatically with the widespread use of reperfusion therapies but may occur in 2–3% of ST-elevation myocardial infarction patients, and mortality is very high if not properly diagnosed, as surgery is the only effective treatment. Echocardiography is the most important tool for diagnosis that should be suspected in patients with hypotension, heart failure, or recurrent chest pain. Awareness and well-established protocols are crucial for an early diagnosis. Modern imaging techniques permit a more reliable and direct identification of left ventricular free wall rupture, which is almost impossible to identify with conventional echocardiography. Mitral regurgitation, secondary to papillary muscle ischaemia or necrosis or left ventricular dilatation and remodelling, without papillary muscle rupture, is frequent after myocardial infarction and is considered as an independent risk factor for outcomes. Revascularization to control ischaemia and surgical repair should be considered in all patients with severe or symptomatic mitral regurgitation in the absence of severe left ventricular dysfunction. Other mechanical complications include true aneurysms and thrombus formation in the left ventricle. Again, these complications have decreased with the use of early reperfusion therapies and, for thrombus formation, with aggressive antithrombotic treatment. In a single large randomized trial (STICH), surgical remodelling of the left ventricle failed to demonstrate a significant improvement in outcomes, although it still may be an option in selected patients.
15
López-Sendón, José, i Esteban López de Sá. Mechanical complications of myocardial infarction. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0045_update_002.
Pełny tekst źródłaStreszczenie:
Mechanical complications after an acute infarction include different forms of heart rupture, including free wall rupture, interventricular septal rupture, and papillary muscle rupture. Its incidence decreased dramatically with the widespread use of reperfusion therapies but may occur in 2–3% of ST-elevation myocardial infarction patients, and mortality is very high if not properly diagnosed, as surgery is the only effective treatment. Echocardiography is the most important tool for diagnosis that should be suspected in patients with hypotension, heart failure, or recurrent chest pain. Awareness and well-established protocols are crucial for an early diagnosis. Modern imaging techniques permit a more reliable and direct identification of left ventricular free wall rupture, which is almost impossible to identify with conventional echocardiography. Mitral regurgitation, secondary to papillary muscle ischaemia or necrosis or left ventricular dilatation and remodelling, without papillary muscle rupture, is frequent after myocardial infarction and is considered as an independent risk factor for outcomes. Revascularization to control ischaemia and surgical repair should be considered in all patients with severe or symptomatic mitral regurgitation in the absence of severe left ventricular dysfunction. Other mechanical complications include true aneurysms and thrombus formation in the left ventricle. Again, these complications have decreased with the use of early reperfusion therapies and, for thrombus formation, with aggressive antithrombotic treatment. In a single large randomized trial (STICH), surgical remodelling of the left ventricle failed to demonstrate a significant improvement in outcomes, although it still may be an option in selected patients.
16
López-Sendón, José, i Esteban López de Sá. Mechanical complications of myocardial infarction. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0045_update_003.
Pełny tekst źródłaStreszczenie:
Mechanical complications after an acute infarction involve different forms of heart rupture, including free wall rupture, interventricular septal rupture, and papillary muscle rupture. Its incidence decreased dramatically with the widespread use of reperfusion therapies occurring in <1% of ST-elevation myocardial infarction patients, and mortality is very high if not properly diagnosed, as surgery is the only effective treatment (Ibanez et al, 2017). Echocardiography is the most important tool for diagnosis that should be suspected in patients with hypotension, heart failure, or recurrent chest pain. Awareness and well-established protocols are crucial for an early diagnosis. Modern imaging techniques permit a more reliable and direct identification of left ventricular free wall rupture, which is almost impossible to identify with conventional echocardiography. Mitral regurgitation, secondary to papillary muscle ischaemia or necrosis or left ventricular dilatation and remodelling, without papillary muscle rupture, is frequent after myocardial infarction and is considered as an independent risk factor for outcomes. Revascularization to control ischaemia and surgical repair should be considered in all patients with severe or symptomatic mitral regurgitation in the absence of severe left ventricular dysfunction. Other mechanical complications include true aneurysms and thrombus formation in the left ventricle. Again, these complications have decreased with the use of early reperfusion therapies and, for thrombus formation, with aggressive antithrombotic treatment. In a single large randomized trial (STICH), surgical remodelling of the left ventricle failed to demonstrate a significant improvement in outcomes, although it still may be an option in selected patients.
17
Pepper, John. Cardioprotection During Cardiac Surgery. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199544769.003.0007.
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• Overall early mortality for cardiac surgery is low at 2–3% but in high risk patients it can be high as 10–15%• The demography of cardiac surgical patients is changing to older and sicker patients• Myocardial ischaemia-reperfusion injury and the systemic inflammatory response are closely related• Several pharmacological agents that have been demon-strated to confer cardioprotection in the experimental setting have been applied to the clinical setting of cardiac surgery. However, the transfer of these findings from the bench to the bedside has been largely disappointing• Potential cardioprotective strategies include pharma-cological agents such as adenosine, and mechanical interventional strategies such as acute normovolaemic haemodilution and remote ischaemic preconditioning.
18
Giacca, Mauro, i Borja Ibáñez. Advanced therapies to treat cardiovascular diseases: controversies and perspectives. Redaktorzy José Maria Pérez-Pomares, Robert G. Kelly, Maurice van den Hoff, José Luis de la Pompa, David Sedmera, Cristina Basso i Deborah Henderson. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198757269.003.0028.
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There is a pressing need to develop novel therapies for myocardial infarction and heart failure, two conditions that affect over 20% of the world population. Despite important advances in achieving revascularization of the ischaemic myocardium and the usefulness of devices in assisting failing hearts, therapy for these conditions remains poor. The final extent of myocardial tissue loss after infarction is a major determinant of post-infarction mortality due to heart failure. In this chapter we review the current strategies aimed at counteracting injury due to acute myocardial ischaemia–reperfusion and the experimental approaches to achieve cardiac and vascular regeneration once damage has occurred. We critically discuss the possibility of inducing tissue restoration by gene transfer or exogenous cell implantation, and report on the exciting possibility of stimulating the endogenous capacity of cardiac regeneration using growth factors and small regulatory RNAs.
19
Jain, Shilpa, i Mark T. Gladwin. Sickle crisis in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0275.
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Sickle cell disease crises are precipitated by an acute occlusion of microvessels, which can lead to end organ ischaemia reperfusion injury and acute haemolysis. Acute fat emboli syndrome, acute lung injury (the acute chest syndrome), acute pulmonary hypertension, and cor pulmonale, haemorrhagic and occlusive stroke, and systemic infection represent the most common life-threatening complications observed in current ICU practice. General principles of management in all patients admitted to the critical care unit are hydration, antibiotics, pain control, and maintenance of oxygenation and ventilation. Red blood cell transfusion therapy is the treatment of choice for most complications of sickle cell disease requiring intensive care management. Transfusion of sickle negative, leukoreduced red blood cells, phenotypically matched for Rhesus and Kell antigens is the minimum standard of care in sickle cell disease patients as they have a high incidence of red blood cell alloimmunization.
20
Bouchama, Abderrezak. Pathophysiology and management of hyperthermia. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0353.
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Hyperthermia is a state of elevated core temperature that rises rapidly above 40°C, secondary to failure of thermoregulation. Hyperthermia has many causes, but it is the hallmark of three conditions—heatstroke, malignant hyperthermia, and neuroleptic malignant syndrome. The clinical and metabolic alterations of hyperthermia, if left untreated, can culminate in multiple organ system failure and death. High temperature causes direct cellular death and tissue damage. The extent of tissue injury is a function of the degree and duration of hyperthermia. Heat-induced ischaemia-reperfusion injury, and exacerbated activation of inflammation and coagulation are also contributory. Hyperthermia is a true medical emergency with rapid progression to multiple organ system failure and death. The primary therapeutic goal is to reduce body temperature as quickly as possible using physical cooling methods, and if indicated, the use of pharmacological treatment to accelerate cooling. There is no evidence of the superiority of one cooling technique over another. Non-invasive techniques that are easy to use and well-tolerated are preferred. Pharmacological cooling with Dantrolene sodium is crucial in the treatment of malignant hyperthermia.
21
Ho, Vanessa P., i Philip S. Barie. Acute acalculous cholecystitis in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0188.
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Acute acalculous cholecystitis (AAC) may occur in surgical or injured, critically-ill, and systemically-ill patients, with diabetes mellitus, malignant disease, abdominal vasculitis, congestive heart failure, cholesterol embolization, shock, and cardiac arrest. Children may also be affected, especially following a viral illness. The pathogenesis of AAC is complex and multifactorial. Ischaemia/reperfusion injury and the associated pro-inflammatory response and oxidative tissue stress, appear to be the central mechanisms, but bile stasis, opioid therapy, positive-pressure ventilation, and parenteral nutrition may all contribute to development of the disease. Ultrasound of the gallbladder is most accurate for the diagnosis of AAC in the critically-ill patient. Computed tomography is probably of comparable accuracy, but carries both advantages and disadvantages. Percutaneous cholecystostomy is now the treatment of choice, controlling AAC in about 85% of patients, despite the known high prevalence of gallbladder infarction (~50%) and perforation (~10%). Rapid improvement may be expected when AAC is diagnosed correctly and cholecystostomy is performed timely. The mortality (historically ~30%) of percutaneous and open cholecystostomy are similar, reflecting the severity of illness, but improved resuscitation and critical care may portend a decreased risk of death.
22
Torbicki, Adam, Marcin Kurzyna i Stavros Konstantinides. Pulmonary embolism. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0066.
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Pulmonary embolism is usually a consequence of deep vein thrombosis, and together the two conditions are known as venous thromboembolism. Non-thromboembolic causes of pulmonary embolism are rare. Pulmonary thromboembolism is a potentially life-threatening disease, if left untreated. This is due to a natural tendency towards early recurrence of pulmonary emboli which may lead to fatal right ventricular failure. In more severe cases, secondary right ventricular failure may result from myocardial ischaemia and injury caused by systemic hypotension and adrenergic overstimulation. Clinical presentation of pulmonary embolism is non-specific and may include dyspnoea, chest pain, haemoptysis, syncope, hypotension, and shock. Patients with suggestive history, symptoms, and signs require an immediate triage which determines further management strategy. Computerized tomographic angiography has become the mainstay of diagnosis. However, depending on the clinical presentation, treatment decisions may also be made based on results from other tests. In particular, in high-risk patients with persistent hypotension or shock, bedside echocardiography may be the only available test to identify patients in need of primary thrombolysis, surgical embolectomy, or percutaneous intervention which will stabilize the systemic cardiac output. For most normotensive patients, anticoagulation is sufficient as initial treatment. However, in the presence of signs of right ventricular dysfunction and myocardial injury monitoring is recommended to allow prompt rescue reperfusion therapy in case of haemodynamic decompensation.
23
Torbicki, Adam, Marcin Kurzyna i Stavros Konstantinides. Pulmonary embolism. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199687039.003.0066_update_001.
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Pulmonary embolism is usually a consequence of deep vein thrombosis, and together the two conditions are known as venous thromboembolism. Non-thromboembolic causes of pulmonary embolism are rare. Pulmonary thromboembolism is a potentially life-threatening disease, if left untreated. This is due to a natural tendency towards early recurrence of pulmonary emboli which may lead to fatal right ventricular failure. In more severe cases, secondary right ventricular failure may result from myocardial ischaemia and injury caused by systemic hypotension and adrenergic overstimulation. Clinical presentation of pulmonary embolism is non-specific and may include dyspnoea, chest pain, haemoptysis, syncope, hypotension, and shock. Patients with suggestive history, symptoms, and signs require an immediate triage which determines further management strategy. Computerized tomographic angiography has become the mainstay of diagnosis. However, depending on the clinical presentation, treatment decisions may also be made based on results from other tests. In particular, in high-risk patients with persistent hypotension or shock, bedside echocardiography may be the only available test to identify patients in need of primary thrombolysis, surgical embolectomy, or percutaneous intervention which will stabilize the systemic cardiac output. For most normotensive patients, anticoagulation is sufficient as initial treatment. However, in the presence of signs of right ventricular dysfunction and myocardial injury monitoring is recommended to allow prompt rescue reperfusion therapy in case of haemodynamic decompensation.
24
Torbicki, Adam, Marcin Kurzyna i Stavros Konstantinides. Pulmonary embolism. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0066_update_002.
Pełny tekst źródłaStreszczenie:
Pulmonary embolism is usually a consequence of deep vein thrombosis, and together the two conditions are known as venous thromboembolism. Non-thromboembolic causes of pulmonary embolism are rare. Pulmonary thromboembolism is a potentially life-threatening disease, if left untreated. This is due to a natural tendency towards early recurrence of pulmonary emboli which may lead to fatal right ventricular failure. In more severe cases, secondary right ventricular failure may result from myocardial ischaemia and injury caused by systemic hypotension and adrenergic overstimulation. Clinical presentation of pulmonary embolism is non-specific and may include dyspnoea, chest pain, haemoptysis, syncope, hypotension, and shock. Patients with suggestive history, symptoms, and signs require an immediate triage which determines further management strategy. Computerized tomographic angiography has become the mainstay of diagnosis. However, depending on the clinical presentation, treatment decisions may also be made based on results from other tests. In particular, in high-risk patients with persistent hypotension or shock, bedside echocardiography may be the only available test to identify patients in need of primary thrombolysis, surgical embolectomy, or percutaneous intervention which will stabilize the systemic cardiac output. For most normotensive patients, anticoagulation is sufficient as initial treatment. However, in the presence of signs of right ventricular dysfunction and myocardial injury monitoring is recommended to allow prompt rescue reperfusion therapy in case of haemodynamic decompensation.
25
Torbicki, Adam, Marcin Kurzyna i Stavros Konstantinides. Pulmonary embolism. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0066_update_003.
Pełny tekst źródłaStreszczenie:
Pulmonary embolism is usually a consequence of deep vein thrombosis, and together the two conditions are known as venous thromboembolism. Non-thromboembolic causes of pulmonary embolism are rare. Pulmonary thromboembolism is a potentially life-threatening disease, if left untreated. This is due to a natural tendency towards early recurrence of pulmonary emboli which may lead to fatal right ventricular failure. In more severe cases, secondary right ventricular failure may result from myocardial ischaemia and injury caused by systemic hypotension and adrenergic overstimulation. Clinical presentation of pulmonary embolism is non-specific and may include dyspnoea, chest pain, haemoptysis, syncope, hypotension, and shock. Patients with suggestive history, symptoms, and signs require an immediate triage which determines further management strategy. Computerized tomographic angiography has become the mainstay of diagnosis. However, depending on the clinical presentation, treatment decisions may also be made based on results from other tests. In particular, in high-risk patients with persistent hypotension or shock, bedside echocardiography may be the only available test to identify patients in need of primary thrombolysis, surgical embolectomy, or percutaneous intervention which will stabilize the systemic cardiac output. For most normotensive patients, anticoagulation is sufficient as initial treatment. However, in the presence of signs of right ventricular dysfunction and myocardial injury monitoring is recommended to allow prompt rescue reperfusion therapy in case of haemodynamic decompensation.
26
Kočka, Viktor, Steen Dalby Kristensen, William Wijns, Petr Toušek i Petr Widimský. Percutaneous coronary interventions in acute coronary syndromes. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0047.
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Three different guidelines of the European Society of Cardiology cover the field of percutaneous coronary interventions. Their main recommendations are the following:All patients with an ST-segment elevation myocardial infarction should undergo immediate coronary angiography and percutaneous coronary intervention as soon as possible after the first medical contact. Thrombolysis can be used as an alternative reperfusion therapy if the time delay to primary percutaneous coronary intervention is more than 2 hoursPatients with very high-risk non-ST-segment elevation acute coronary syndromes (recurrent or ongoing chest pain, profound or dynamic electrocardiogram changes, major arrhythmias, or haemodynamic instability) should undergo urgent coronary angiography within less than 2 hours after the initial hospital admissionAll moderate- to high-risk (GRACE score >140 or at least one primary high-risk criterion) non-ST-segment elevation acute coronary syndromes patients should undergo coronary angiography before discharge; the ideal timing is within 24 hours after admission for high-risk groups, and within 72 hours for moderate-risk groupsOther patients with recurrent symptoms or at least one high-risk criterion should undergo coronary angiography within 72 hours of first presentationLow-risk non-ST-segment elevation acute coronary syndromes may be treated conservatively, and the indication for an invasive evaluation can be done, based on the evidence of ischaemia during exercise stress testingStents should be used during all percutaneous coronary intervention procedures, whenever technically feasible. Second-generation drug-eluting stents do not increase stent thrombosis and can be safely used in the ST-segment elevation myocardial infarction and non-ST-segment elevation acute coronary syndrome settingsTriple pharmacotherapy, consisting of aspirin, thienopyridine antiplatelet agent, and anticoagulation with heparin or bivalirudin, should be used in all percutaneous coronary intervention procedures, with glycoprotein IIb/IIIa inhibitors added in patients with a high thrombus burden and low bleeding risk
27
Kočka, Viktor, Steen Dalby Kristensen, William Wijns, Petr Toušek i Petr Widimský. Percutaneous coronary interventions in acute coronary syndromes. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199687039.003.0047_update_001.
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Three different guidelines of the European Society of Cardiology cover the field of percutaneous coronary interventions. Their main recommendations are the following:All patients with an ST-segment elevation myocardial infarction should undergo immediate coronary angiography and percutaneous coronary intervention as soon as possible after the first medical contact. Thrombolysis can be used as an alternative reperfusion therapy if the time delay to primary percutaneous coronary intervention is more than 2 hoursPatients with very high-risk non-ST-segment elevation acute coronary syndromes (recurrent or ongoing chest pain, profound or dynamic electrocardiogram changes, major arrhythmias, or haemodynamic instability) should undergo urgent coronary angiography within less than 2 hours after the initial hospital admissionAll moderate- to high-risk (GRACE score >140 or at least one primary high-risk criterion) non-ST-segment elevation acute coronary syndromes patients should undergo coronary angiography before discharge; the ideal timing is within 24 hours after admission for high-risk groups, and within 72 hours for moderate-risk groupsOther patients with recurrent symptoms or at least one high-risk criterion should undergo coronary angiography within 72 hours of first presentationLow-risk non-ST-segment elevation acute coronary syndromes may be treated conservatively, and the indication for an invasive evaluation can be done, based on the evidence of ischaemia during exercise stress testingStents should be used during all percutaneous coronary intervention procedures, whenever technically feasible. Second-generation drug-eluting stents do not increase stent thrombosis and can be safely used in the ST-segment elevation myocardial infarction and non-ST-segment elevation acute coronary syndrome settingsTriple pharmacotherapy, consisting of aspirin, thienopyridine antiplatelet agent, and anticoagulation with heparin or bivalirudin, should be used in all percutaneous coronary intervention procedures, with glycoprotein IIb/IIIa inhibitors added in patients with a high thrombus burden and low bleeding risk
28
Kočka, Viktor, Steen Dalby Kristensen, William Wijns, Petr Toušek i Petr Widimský. Percutaneous coronary interventions in acute coronary syndromes. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0047_update_002.
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Three different guidelines of the European Society of Cardiology cover the field of percutaneous coronary interventions. Their main recommendations are the following: All patients with an ST-segment elevation myocardial infarction should undergo immediate coronary angiography and percutaneous coronary intervention as soon as possible after the first medical contact. Thrombolysis can be used as an alternative reperfusion therapy if the time delay to primary percutaneous coronary intervention is more than 2 hours. Patients with very high-risk non-ST-segment elevation acute coronary syndromes (recurrent or ongoing chest pain, profound or dynamic electrocardiogram changes, major arrhythmias, or haemodynamic instability) should undergo urgent coronary angiography within less than 2 hours after the initial hospital admissionAll moderate- to high-risk (GRACE score >140 or at least one primary high-risk criterion) non-ST-segment elevation acute coronary syndromes patients should undergo coronary angiography before discharge; the ideal timing is within 24 hours after admission for high-risk groups, and within 72 hours for moderate-risk groups. Other patients with recurrent symptoms or at least one high-risk criterion should undergo coronary angiography within 72 hours of first presentation. Low-risk non-ST-segment elevation acute coronary syndromes may be treated conservatively, and the indication for an invasive evaluation can be done, based on the evidence of ischaemia during exercise stress testing. Stents should be used during all percutaneous coronary intervention procedures, whenever technically feasible. Second-generation drug-eluting stents do not increase stent thrombosis and can be safely used in the ST-segment elevation myocardial infarction and non-ST-segment elevation acute coronary syndrome settings. Triple pharmacotherapy, consisting of aspirin, thienopyridine antiplatelet agent, and anticoagulation with heparin or bivalirudin, should be used in all percutaneous coronary intervention procedures, with glycoprotein IIb/IIIa inhibitors added in patients with a high thrombus burden and low bleeding risk.
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Kočka, Viktor, Steen Dalby Kristensen, William Wijns, Petr Toušek i Petr Widimský. Percutaneous coronary interventions in acute coronary syndromes. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0047_update_003.
Pełny tekst źródłaStreszczenie:
Three different guidelines of the European Society of Cardiology cover the field of percutaneous coronary interventions. Their main recommendations are the following: All patients with an ST-segment elevation myocardial infarction should undergo immediate coronary angiography and percutaneous coronary intervention as soon as possible after the first medical contact. Thrombolysis can be used as an alternative reperfusion therapy if the time delay to primary percutaneous coronary intervention is more than 2 hours. Patients with very high-risk non-ST-segment elevation acute coronary syndromes (recurrent or ongoing chest pain, profound or dynamic electrocardiogram changes, major arrhythmias, or haemodynamic instability) should undergo urgent coronary angiography within less than 2 hours after the initial hospital admissionAll moderate- to high-risk (GRACE score >140 or at least one primary high-risk criterion) non-ST-segment elevation acute coronary syndromes patients should undergo coronary angiography before discharge; the ideal timing is within 24 hours after admission for high-risk groups, and within 72 hours for moderate-risk groups. Other patients with recurrent symptoms or at least one high-risk criterion should undergo coronary angiography within 72 hours of first presentation. Low-risk non-ST-segment elevation acute coronary syndromes may be treated conservatively, and the indication for an invasive evaluation can be done, based on the evidence of ischaemia during exercise stress testing. Stents should be used during all percutaneous coronary intervention procedures, whenever technically feasible. Second-generation drug-eluting stents do not increase stent thrombosis and can be safely used in the ST-segment elevation myocardial infarction and non-ST-segment elevation acute coronary syndrome settings. Triple pharmacotherapy, consisting of aspirin, thienopyridine antiplatelet agent, and anticoagulation with heparin or bivalirudin, should be used in all percutaneous coronary intervention procedures, with glycoprotein IIb/IIIa inhibitors added in patients with a high thrombus burden and low bleeding risk.
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Sever, Mehmet Şükrü, i Raymond Vanholder. Acute kidney injury in polytrauma and rhabdomyolysis. Redaktor Norbert Lameire. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0252_update_001.
Pełny tekst źródłaStreszczenie:
The term ‘polytrauma’ refers to blunt (or crush) trauma that involves multiple body regions or cavities, and compromises physiology to potentially cause dysfunction of uninjured organs. Polytrauma frequently affects muscles resulting in rhabdomyolysis. In daily life, it mostly occurs after motor vehicle accidents, influencing a limited number of patients; after mass disasters, however, thousands of polytrauma victims may present at once with only surgical features or with additional medical complications (crush syndrome). Among the medical complications, acute kidney injury (AKI) deserves special mention, since it is frequent and has a substantial impact on the ultimate outcome.Several factors play a role in the pathogenesis of polytrauma (or crush)-induced AKI: (1) hypoperfusion of the kidneys, (2) myoglobin-induced direct nephrotoxicity, and intratubular obstruction, and also (3) several other mechanisms (i.e. iron and free radical-induced damage, disseminated intravascular coagulation, and ischaemia reperfusion injury). Crush-related AKI is prerenal at the beginning; however, acute tubular necrosis may develop eventually. In patients with crush syndrome, apart from findings of trauma, clinical features may include (but are not limited to) hypotension, oliguria, brownish discoloration of urine, and other symptoms and findings, such as sepsis, acute respiratory distress syndrome, disseminated intravascular coagulation, bleeding, cardiac failure, arrhythmias, electrolyte disturbances, and also psychological trauma.In the biochemical evaluation, life-threatening hyperkalaemia, retention of uraemic toxins, high anion gap metabolic acidosis, elevated serum levels of myoglobin, and muscle enzymes are noted; creatine phosphokinase is very useful for diagnosing rhabdomyolysis.Early fluid administration is vital to prevent crush-related AKI; the rate of initial fluid volume should be 1000 mL/hour. Overall, 3–6 L are administered within a 6-hour period considering environmental, demographic and clinical features, and urinary response to fluids. In disaster circumstances, the preferred fluid formulation is isotonic saline because of its ready availability. Alkaline (bicarbonate-added) hypotonic saline may be more useful, especially in isolated cases not related to disaster, as it may prevent intratubular myoglobin, and uric acid plugs, metabolic acidosis, and also life-threatening hyperkalaemia.In the case of established acute tubular necrosis, dialysis support is life-saving. Although all types of dialysis techniques may be used, intermittent haemodialysis is the preferred modality because of medical and logistic advantages. Close follow-up and appropriate treatment improve mortality rates, which may be as low as 15–20% even in disaster circumstances. Polytrauma victims after mass disasters deserve special mention, because crush syndrome is the second most frequent cause of death after trauma. Chaos, overwhelming number of patients, and logistical drawbacks often result in delayed, and sometimes incorrect treatment. Medical and logistical disaster preparedness is useful to improve the ultimate outcome of disaster victims.