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1

Pharm, Boucher Michel B., and Canadian Coordinating Office for Health Technology Assessment., eds. The role of clopidogrel in the secondary prevention of recurrent ischemic vascular events after acute myocardial ischemia: A critical appraisal of the CURE Trial. Ottawa, Ont: Canadian Coordinating Office for Health Technology Assessment, 2002.

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2

L, Jones, and National Co-ordinating Centre for HTA (Great Britain), eds. Clinical effectiveness and cost-effectiveness of clopidogrel and modified-release dipyridamole in the secondary prevention of occlusive vascular events: A systematic review and economic evaluation. Tunbridge Wells: Published by Gray Publishing on behalf of NCCTHA, 2004.

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3

Sprynger, Muriel, Iana Simova, and Scipione Carerj. Vascular echo imaging. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198726012.003.0068.

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Arterial diseases are heavily intertwined with atherosclerosis and coronary artery disease and the presence of both symptomatic and asymptomatic peripheral artery diseases is known to affect the rate of cardiovascular events and deaths. Screening for abdominal aortic aneurysm (AAA) in selected populations is also a major issue for the cardiologist. Additionally, intima-media thickness and ankle-brachial index (ABI) measurements, screening for carotid or femoral plaques, and new techniques looking at the rigidity and elasticity of arteries may further help with risk stratification, especially in intermediary risk populations. Cardiologists may also encounter other conditions such as subclavian artery disease, arterial dissection, arterial entrapment, and arteritis (e.g. giant cell or Takayasu’s arteritis). Even if they don’t undertake imaging themselves, they should know about these diseases and when to refer patients. Although cardiac and vascular ultrasounds are complementary, they require a completely different skill set and formal training. The ultimate goal of this chapter is to define the basic principles that any cardiologist should know, and also provide guidance to cardiologists more interested in vascular diseases. For the benefit of the patient there is a need for collaboration between the different disciplines involved in vascular diseases according to local medical availability and skill.
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4

Delcourt, Candice, and Craig Anderson. Epidemiology of stroke. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0234.

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Approximately 20 million strokes occur in the world each year and over one-quarter of these are fatal. This makes stroke the second most common cause of death, after ischaemic heart disease, and strokes are responsible for 6 million deaths (almost 10% of all deaths) annually. Stroke has major consequences in terms of residual physical disability, depression, dementia, epilepsy, and carer burden. Moreover, around 20% of survivors experience a further stroke or serious vascular event within a few years of the index event. The economic and societal costs of stroke are enormous. With ongoing demographic changes, including the ageing and urbanization of populations, and persistence of highly prevalent risk factors related to adverse lifestyles, the global burden of disease related to stroke is predicted to rise substantially by 2030.
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5

Scolding, Neil. Vasculitis and collagen vascular diseases. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0862.

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That part of the clinical interface between neurology and general medicine occupied by inflammatory and immunological diseases is neither small nor medically trivial. Neurologists readily accept the challenges of ‘primary’ immune diseases of the nervous system: these tend to be focussed on one particular target such as oligodendrocytes or the neuro-muscular junction present in predictable ways, and are amenable as a rule to rational, methodological diagnosis, and occasionally even treatment. This is proper neurology.‘Secondary’ neurological involvement in diseases mainly considered systemic inflammatory conditions—for example, SLE, sarcoidosis, vasculitis, and Behçet’s—is a rather different matter. It may be difficult enough to secure such a diagnosis even when systemic disease has previously been diagnosed and new neurological features need to be differentiated from iatrogenic disease, particularly drug side effects or the consequences of immune suppression. But all the diseases mentioned may present with and confine themselves wholly to the nervous system; they may mimic one another, and pursue erratic and unpredictable clinical courses. In central nervous system disease, diagnosis by tissue biopsy is potentially hazardous and unattractive. Few neurologists enjoy excesses of confidence or expertise when faced with such clinical problems: the cautious diagnostician is perplexed, and the evidence-based neuroprescriber confounded. Unsurprisingly, great variations in approaches to diagnosis and management are seen (Scolding et al. 2002b).But rheumatologically inclined general, renal or respiratory physicians, comfortable when managing inflammation affecting their system or indeed other parts of the body designed to support the nervous system, are generally also ill at ease when faced with neurological features whose differential diagnosis may be large, particularly given the near universal diagnostic non-specificity of either imaging or CSF analysis.Here then is the subject material for this chapter: the diagnosis and management of central nervous system involvement in inflammatory and immunological systemic diseases (Scolding 1999a). In not one of these neurological conditions has a single controlled therapeutic trial been reported, and much that is published on these conditions is misleading or inaccurate. And yet the frequency with which the diagnosis is only confirmed or even first emerges at autopsy bears stark witness to both the severity and evasiveness of these disorders.
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6

Jones, Bryn. Complications of total knee replacement. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199550647.003.008007.

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♦ 81–89% overall patient satisfaction following total knee replacement♦ 1 in 8 patients experience unexplained postoperative pain♦ Obesity, increasing age, and medical comorbidities increase the risk of postoperative complications♦ Prosthetic infection rate at 1 year is 1–2%♦ Preoperative range of movement often determines postoperative range♦ Low risk of acute vascular event and neurological and ligamentous injury♦ Duration and method of venous thromboprophylaxis remains controversial♦ Periprosthetic femoral and tibial fractures require stabilisation. Fixation of periprosthetic patella fractures is not recommended♦ New surgical techniques and innovations require long term evaluation.
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7

Vlachopoulos, Charalambos, and Nikolaos Ioakeimidis. Erectile dysfunction as a marker and predictor of cardiovascular disease. Edited by Charalambos Vlachopoulos. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0245.

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Erectile dysfunction (ED) is defined as the inability to obtain or maintain a penile erection to support satisfactory sexual performance. It is considered an early manifestation of generalized vascular disease and recognized as a marker of increased cardiovascular risk both acutely and chronically by predicting all-cause mortality, cardiovascular mortality, coronary events, stroke, and peripheral artery disease in men with and without known coronary artery disease. The link between ED and cardiovascular disease might reside in the interaction between androgen level, chronic inflammation, and cardiovascular risk factors that determine endothelial dysfunction and atherosclerosis both in the penile and coronary circulation. Because penile artery size is smaller compared with coronary arteries, the same degree of endothelial dysfunction and atherosclerotic burden causes a more significant reduction of blood flow in erectile tissues compared with that in coronary circulation. From a clinical standpoint, because ED may precede cardiovascular disease, it can be used as an early marker to identify men at higher risk of cardiovascular events. The average 3-year time period between the onset of ED symptoms and a cardiovascular event offers the opportunity for detailed cardiological assessment and intensive treatment of risk factors.
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8

Delcourt, Candice, and Craig Anderson. Diagnosis and assessment of stroke. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0235.

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Approximately 20 million strokes occur in the world each year and over one-quarter of these are fatal. This makes stroke the second most common cause of death, after ischaemic heart disease, and strokes are responsible for 6 million deaths (almost 10% of all deaths) annually. Stroke has major consequences in terms of residual physical disability, depression, dementia, epilepsy, and carer burden. Moreover, around 20% of survivors experience a further stroke or serious vascular event within a few years of the index event. Ischaemic stroke contributes the greatest share of the impact of stroke, with a rate of approximately 1 in 1000 person-years and accounting for between 60% (in Asia) and 90% (in Western ‘white’ populations) of all strokes around the world. Diagnosis and assessment are essentially clinical and confirmed by CT or MRI scanning. Prognostication is difficult in the early phase of haemorrhagic stroke and in ischaemic stroke is affected by the availability and timely use of treatments to recanalize the occluded vessel.
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9

O’Leary, Ronan, and Andrew R. Bodenham. Arterial and venous cannulation in the ICU. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0130.

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Despite being almost ubiquitous within the critically- ill population, vascular access remains a frequent cause of iatrogenic injury, manifested as both procedural complications and later events, such as infection and thrombosis. Untoward events are minimized by expert tuition and meticulous practical technique. Consensus guidelines on training in vascular access are discussed. Vascular access, particularly central catheterization, should not be undertaken lightly. Can a patient be managed without vascular access or can the number of vascular access devices be rationalized? Other routes for drug and fluid administration exist, particularly enterally during the recovery phase. This chapter covers vascular access during critical illness and discusses the development of more advanced techniques.
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10

Leys, Didier, Charlotte Cordonnier, and Valeria Caso. Stroke. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0067.

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Stroke is a major public health issue. Many are treatable in the acute stage, provided patients are admitted soon enough. The overall incidence of stroke in Western countries is approximately 2400 per year per million inhabitants, and 80% are due to cerebral ischaemia. The prevalence is approximately 12 000 per million inhabitants. Stroke is associated with increased long-term mortality, handicap, cognitive and behavioural impairments, recurrence, and an increased risk of other types of vascular events. It is of major interest to take the heterogeneity of stroke into account, because of differences in the acute management, secondary prevention, and outcomes, according to the subtype and cause of stroke. In all types of stroke, early epileptic seizures, delirium, increased intracranial pressure, and non-specific complications are frequent. In ischaemic strokes, specific complications, such as malignant infarcts, spontaneous haemorrhagic transformation, early recurrence, and a new ischaemic event in another vascular territory, are frequent. In haemorrhagic strokes, the major complication is the subsequent increased volume of bleeding. There is strong evidence that stroke patients should be treated in dedicated stroke units; each time 24 patients are treated in a stroke unit, instead of a conventional ward, one death and one dependence are prevented. This effect does not depend on age, severity, and the stroke subtype. For this reason, stroke unit care is the cornerstone of the treatment of stroke, aiming at the detection and management of life-threatening emergencies, stabilization of most physiological parameters, and prevention of early complications. In ischaemic strokes, besides this general management, specific therapies include intravenous recombinant tissue plasminogen activator, given as soon as possible and before 4.5 hours, otherwise aspirin 300 mg, immediately or after 24 hours in case of thrombolysis, and, in a few patients, decompressive surgery. In intracerebral haemorrhages, blood pressure lowering and haemostatic therapy, when needed, are the two targets, but surgery does not seem effective to reduce death and disability.
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11

Leys, Didier, Charlotte Cordonnier, and Valeria Caso. Stroke. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199687039.003.0067_update_001.

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Stroke is a major public health issue. Many are treatable in the acute stage, provided patients are admitted soon enough. The overall incidence of stroke in Western countries is approximately 2400 per year per million inhabitants, and 80% are due to cerebral ischaemia. The prevalence is approximately 12 000 per million inhabitants. Stroke is associated with increased long-term mortality, handicap, cognitive and behavioural impairments, recurrence, and an increased risk of other types of vascular events. It is of major interest to take the heterogeneity of stroke into account, because of differences in the acute management, secondary prevention, and outcomes, according to the subtype and cause of stroke. In all types of stroke, early epileptic seizures, delirium, increased intracranial pressure, and non-specific complications are frequent. In ischaemic strokes, specific complications, such as malignant infarcts, spontaneous haemorrhagic transformation, early recurrence, and a new ischaemic event in another vascular territory, are frequent. In haemorrhagic strokes, the major complication is the subsequent increased volume of bleeding. There is strong evidence that stroke patients should be treated in dedicated stroke units; each time 24 patients are treated in a stroke unit, instead of a conventional ward, one death and one dependence are prevented. This effect does not depend on age, severity, and the stroke subtype. For this reason, stroke unit care is the cornerstone of the treatment of stroke, aiming at the detection and management of life-threatening emergencies, stabilization of most physiological parameters, and prevention of early complications. In ischaemic strokes, besides this general management, specific therapies include intravenous recombinant tissue plasminogen activator, given as soon as possible and before 4.5 hours, otherwise aspirin 300 mg, immediately or after 24 hours in case of thrombolysis, and, in a few patients, decompressive surgery. In intracerebral haemorrhages, blood pressure lowering and haemostatic therapy, when needed, are the two targets, but surgery does not seem effective to reduce death and disability.
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12

Leys, Didier, Charlotte Cordonnier, and Valeria Caso. Stroke. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0067_update_002.

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Stroke is a major public health issue. Many are treatable in the acute stage, provided patients are admitted soon enough. The overall incidence of stroke in Western countries is approximately 2400 per year per million inhabitants, and 80% are due to cerebral ischaemia. The prevalence is approximately 12 000 per million inhabitants. Stroke is associated with increased long-term mortality, handicap, cognitive and behavioural impairments, recurrence, and an increased risk of other types of vascular events. It is of major interest to take the heterogeneity of stroke into account, because of differences in the acute management, secondary prevention, and outcomes, according to the subtype and cause of stroke. In all types of stroke, early epileptic seizures, delirium, increased intracranial pressure, and non-specific complications are frequent. In ischaemic strokes, specific complications, such as malignant infarcts, spontaneous haemorrhagic transformation, early recurrence, and a new ischaemic event in another vascular territory, are frequent. In haemorrhagic strokes, the major complication is the subsequent increased volume of bleeding. There is strong evidence that stroke patients should be treated in dedicated stroke units; each time 24 patients are treated in a stroke unit, instead of a conventional ward, one death and one dependence are prevented. This effect does not depend on age, severity, and the stroke subtype. For this reason, stroke unit care is the cornerstone of the treatment of stroke, aiming at the detection and management of life-threatening emergencies, stabilization of most physiological parameters, and prevention of early complications. In ischaemic strokes, besides this general management, specific therapies include intravenous recombinant tissue plasminogen activator, given as soon as possible and before 4.5 hours, mechanical thrombectomy in case of proximal occlusion (middle cerebral artery, intracranial internal carotid artery, basilar artery), on top of thrombolysis in the absence of contraindication or alone otherwise, aspirin 300 mg, immediately or after 24 hours in case of thrombolysis, and, in a few patients, decompressive surgery. In intracerebral haemorrhages, blood pressure lowering and haemostatic therapy, when needed, are the two targets, while surgery does not seem effective to reduce death and disability.
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13

Chong, Ji Y., and Michael P. Lerario. Forget About It. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190495541.003.0037.

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Cognitive impairment is common following stroke. The clinical course and presentation are variable in vascular dementia, but the diagnosis can often be tied to recent vascular events or to progressive white matter lesions on MRI. Because there is considerable overlap between patients with vascular and Alzheimer’s type dementia, both acetylcholinesterase inhibitors and memantine have been tried off-label to treat the cognitive symptoms of vascular dementia with mixed results.
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14

Alchi, Bassam, and David Jayne. The patient with antiphospholipid syndrome with or without lupus. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0164.

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Antiphospholipid syndrome (APS) is an autoimmune disorder characterized by recurrent arterial or venous thrombosis and/or pregnancy loss, accompanied by laboratory evidence of antiphospholipid antibodies (aPL), namely anticardiolipin antibodies (aCL), lupus anticoagulant (LA), and antibodies directed against beta-2 glycoprotein 1 (β‎‎‎2GP1). APS may occur as a ‘primary’ form, ‘antiphospholipid syndrome,’ without any known systemic disease or may occur in the context of systemic lupus erythematosus (SLE), ‘SLE-related APS’. APS may affect any organ system and displays a broad spectrum of thrombotic manifestations, ranging from isolated lower extremity deep vein thrombosis to the ‘thrombotic storm’ observed in catastrophic antiphospholipid syndrome. Less frequently, patients present with non-thrombotic manifestations (e.g. thrombocytopaenia, livedo reticularis, pulmonary hypertension, valvular heart disease, chorea, and recurrent fetal loss).The kidney is a major target organ in both primary and SLE-related APS. Renal involvement is typically caused by thrombosis occurring at any location within the renal vasculature, leading to diverse effects, depending on the size, type, and site of vessel involved. The renal manifestations of APS include renal artery stenosis and/or renovascular hypertension, renal infarction, APS nephropathy (APSN), renal vein thrombosis, allograft vasculopathy and vascular thrombosis, and thrombosis of dialysis access.Typical vascular lesions of APSN may be acute, the so-called thrombotic microangiopathy, and/or chronic, such as arteriosclerosis, fibrous intimal hyperplasia, tubular thyroidization, and focal cortical atrophy. The spectrum of renal lesions includes non-thrombotic conditions, such as glomerulonephritis. Furthermore, renal manifestations of APS may coexist with other pathologies, especially proliferative lupus nephritis.Early diagnosis of APS requires a high degree of clinical suspicion. The diagnosis requires one clinical (vascular thrombosis or pregnancy morbidity) and at least one laboratory (LA, aCL, and/or anti-β‎‎‎2GP1) criterion, positive on repeated testing.The aetiology of APS is not known. Although aPL are diagnostic of, and pathogenic in, APS, a ‘second hit’ (usually an inflammatory event) may trigger thrombosis in APS. The pathogenesis of the thrombotic tendency in APS remains to be elucidated, but may involve a combination of autoantibody-mediated dysregulation of coagulation, platelet activation, and endothelial injury.Treatment of APS remains centred on anticoagulation; however, it has also included the use of corticosteroids and other immunosuppressive therapy. The prognosis of patients with primary APS is variable and unpredictable. The presence of APS increases morbidity (renal and cerebral) and mortality of SLE patients.
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15

McNally & co. [from old catalog] Rand. Risk of Further Acute Vascular Events Following an Initial Myocardial Infarction or Stroke (Road Safety Research Report). Department for Transport, 2006.

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16

Hajhosseiny, Reza, Kaivan Khavandi, and David J. Goldsmith. Sudden cardiac death in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0108.

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Epidemiological data demonstrate the unique vulnerability of chronic kidney disease (CKD) subjects to cardiovascular disease, the most catastrophic being sudden cardiac death (SCD). In patients with declining kidney function there is a continuum of cardiovascular risk. In those individuals who survive to reach end-stage renal disease (ESRD), the risk of suffering a cardiac event is extremely high. Some of this risk is explained by the common risk factors and traditional cardiovascular events, namely atherosclerotic plaque fissure and rupture, but there is now evidence of a distinct ‘later CKD’ mechanism, notably arrhythmias. This appears particularly true in later stages of CKD and corresponds with the multifaceted range of myocardial and vascular insults operating. The physiological milieu of disordered vessel autoregulation, sequestered vasoprotective agents, loss of conduit and small artery elasticity/compliance, a stiffened and fibrotic myocardium, with calcified and diseased coronary arteries, all within an inflammatory environment, all contribute to arrhythmia generation. The final insult is changes in volume and electrolyte status. Risk stratification tools would be helpful in guiding clinicians to recognize those subjects likely to benefit from specific interventional strategies. These might include the novel, or emerging serum, haemodynamic, or electrocardiographic biomarkers in CKD. Current tools—such as those used for stratifying risk for SCD and determining the need for ICD implantation—are not valid in ESRD patients. Beta blockers appear likely to be generally advisable, blood pressure permitting, for patients with significant cardiomyopathy. Evidence for implantable cardiac defibrillators (ICD) is lacking. There is good reason to think that young dialysis patients at high risk of sudden death may benefit, but the risk/benefit ratio for older patients is less likely to be advantageous. These hypotheses need further investigation.
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17

Levy, David. Macrovascular complications, hypertension, and lipids. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198766452.003.0008.

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Premature vascular disease is common in Type 1 diabetes, especially in women and those with long duration. Many studies have identified early vascular involvement, using carotid Doppler and coronary artery calcification. Symptoms of coronary heart disease are often absent or muted, and the best methods for identifying occult coronary heart disease in Type 1 patients are not known. The concept of ideal cardiovascular health is valuable in planning preventive lifestyle and medical interventions. ‘Essential’ hypertension in young Type 1 patients is common, and reflects increased arterial stiffness. Hypertension is invariable in patients with any degree of albuminuria or renal impairment. Statin treatment in patients over 40 years old is recommended, but the evidence base is weak. Statins and ezetimibe are the only agents of prognostic value currently available for prevention of vascular events. Primary prevention with aspirin needs individual assessment. Insulin resistance/metabolic syndrome is frequent in Type 1 diabetes.
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18

Tanislav, Christian, and Manfred Kaps. Classification. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198722366.003.0003.

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The classification of a cerebrovascular event distils information obtained in the workup and other related case history to a category indicating a specific pathophysiology, with direct implications for the subsequent secondary prevention management. A minimum standard of diagnostics is required for a precise classification. In young stroke victims, the conventional Trial of Org 10172 in Acute Stroke Treatment (TOAST) stroke subtype classification may only address the aetiopathogenesis in 30–60% of the individuals who are affected by vascular risk factors. Applying the criteria defined by TOAST for large-artery atherosclerosis, cardioembolism, and small artery disease is reliable for young stroke victims as verified in many clinical investigations. However, in a considerable proportion of stroke patients, the stroke aetiology remains unclear. For this group, some patients need to be treated in a particular manner, such as those with two or more possible aetiologies or those with suspected paradoxical embolism. In patients remaining purely cryptogenic despite an extensive diagnostic workup, imaging findings may help to identify potential triggers, particularly when an embolic infarction pattern in the acute brain imaging is obvious. Despite its shortcomings, the TOAST classification is the most universally used classification in ischaemic stroke patients. New developments in the field are addressed in this chapter and aspects are incorporated for the nominated classification adapted for the specific group of young stroke patients.
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19

Tombetti, Enrico, and Justin C. Mason. Pathophysiology of vasculitis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0017.

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Vasculitis represents a spectrum of disorders that are often divided on the basis of the predominant vessel size affected into large-, medium- and small-vessel vasculitides. This chapter will focus on the pathogenesis of the anti-neutrophil cytoplasmic antibody (ANCA)-associated medium- and small-vessel vasculitides (AAV), and large-vessel vasculitis, Takayasu arteritis, and giant cell arteritis. Underlying pathogenic mechanisms in vasculitis remain to be fully understood. In particular, the initiating event(s) are not known. A combination of infectious or other environmental triggers on a susceptible genetic background is currently favoured. In addition to the vessel size affected, the mechanisms of vascular injury vary. Moreover, extravascular granulomatosis may play an important role in disease manifestations. The innate and adaptive immune systems contribute to its pathogenesis. Although pathogenic antibodies have not been identified in large-vessel vasculitis, ANCA are directly implicated in small- and medium-vessel AAV. Disease manifestations are varied and diverse and may include arterial stenosis or aneurysms, glomerulonephritis and renal failure, gastro-intestinal, pulmonary, cutaneous, and neurological complications, visual disturbance, deafness, and nasal bridge collapse. Life-threatening cardiovascular disease is also seen, with myocarditis, pericarditis, valvular heart disease, thrombosis, systemic and pulmonary arterial hypertension, and accelerated coronary heart disease all reported. Despite this, the prognosis for patients with vasculitis has improved significantly in recent decades. Further understanding of the pathogenesis of vasculitis will lead to the discovery of further therapeutic targets and novel, safer biologic therapies.
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20

Dodds, Chris, Chandra M. Kumar, and Frédérique Servin. Emergency anaesthesia in the elderly. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198735571.003.0006.

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Emergency surgery in the elderly is needed even if elective surgery would not be considered. Often, it is due to trauma or to intra-abdominal, vascular, or neurosurgical emergencies. The time from onset of the cause of the emergency to operative treatment is directly related to complications and death. Delay to accurate diagnosis is common and may be masked by delirium. Sepsis, pain hypotension, and metabolic disorders may all trigger delirium. Resuscitation and optimization should be concurrent with operative management. Important factors considered include the possible cause of a fall (cardiac/neurologic), likelihood of severe hypovolaemia, electrolyte disorders, and ischaemic vascular disease (occlusive and embolic). Emergency laparotomy is reviewed with the possible reasons behind the appalling outcome data, such as delayed diagnosis and poor nutritional state.
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21

Ferro, José M., and Ana Catarina Fonseca. Secondary prevention. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198722366.003.0015.

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There are no specific guidelines regarding secondary stroke prevention in young adult stroke patients. Recommendations for secondary prevention are mainly extrapolated from data obtained from older individuals, because young adults were excluded or under-represented in most secondary stroke prevention clinical trials. Secondary stroke prevention includes (a) screening and control of vascular risk factors, that is, hypertension, diabetes mellitus, hyperlipidaemia, atrial fibrillation, hormonal contraception, infections, trauma, physical inactivity, obesity, poor nutrition, smoking, alcohol, and illicit drug use; and (b) identification and treatment of specific causes of ischaemic stroke, that is, cardioembolism, large vessel extra- and intracranial atherosclerotic disease, small vessel disease, dissection, antiphospholipid syndrome, moyamoya disease, sickle cell disease, and some rare diseases. There is then an opportunity for lifelong prevention of vascular events after stroke in a young adult.
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22

Badimon, Lina, Felix C. Tanner, Giovanni G. Camici, and Gemma Vilahur. Pathophysiology of thrombosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0018.

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Ischaemic heart disease and stroke are major causes of death and morbidity worldwide. Coronary and cerebrovascular events are mainly a consequence of a sudden thrombotic occlusion of the vessel lumen. Arterial thrombosis usually develops on top of a disrupted atherosclerotic plaque because of the exposure of thrombogenic material, such as collagen fibrils and tissue factor (TF), to the flowing blood. TF, either expressed by subendothelial cells, macrophage- and/or vascular smooth muscle-derived foam-cells in atherosclerotic plaques, is a key element in the initiation of thrombosis due to its ability to induce thrombin formation (a potent platelet agonist) and subsequent fibrin deposition at sites of vascular injury. Adhered platelets at the site of injury also play a crucial role in the pathophysiology of atherothrombosis. Platelet surface receptors (mainly glycoproteins) interact with vascular structures and/or Von Willebrand factor triggering platelet activation signalling events, including an increase in intracellular free Ca2+, exposure of a pro-coagulant surface, and secretion of platelet granule content. On top of this, interaction between soluble agonists and platelet G-coupled protein receptors further amplifies the platelet activation response favouring integrin alpha(IIb)beta(3) activation, an essential step for platelet aggregation. Blood-borne TF and microparticles have also been shown to contribute to thrombus formation and propagation. As thrombus evolves different circulating cells (red-blood cells and leukocytes, along with occasional undifferentiated cells) get recruited in a timely dependent manner to the growing thrombus and further entrapped by the formation of a fibrin mesh.
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23

Steiner, Lisa A. Osteomyelitis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199976805.003.0049.

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Osteomyelitis is an infectious process that affects any part of the bone, including the periosteum, the cortex, or the marrow. It most often occurs in the lower extremities and can be an acute, subacute, or chronic process. Osteomyelitis is often characterized as a consequence of a contiguous spread or hematogenous spread of bacterial infection or as a consequence of vascular insufficiency. Chronic osteomyelitis can be associated with significant bone necrosis, sometimes requiring months to years of treatment with antibiotics or even surgical debridement. Consultation with the orthopedic service (or spine service for vertebral osteomyelitis) should be considered. Vascular service consultation should also occur if there is a concern for osteomyelitis in the foot of a patient with diabetes mellitus. These patients often require admission to the hospital for follow-up.
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24

Carmeliet, Peter, Guy Eelen, and Joanna Kalucka. Arteriogenesis versus angiogenesis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0008.

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Higher organisms have a cardiovascular circulatory system with blood vessels to supply vital nutrients and oxygen to distant tissues. It is therefore not surprising that vascular disorders are leading causes of mortality. Understanding how new blood vessels form, creates opportunities to cure these life-threatening diseases. After birth, growth of blood vessels mainly occurs via two distinct mechanisms depending on the initial trigger: angiogenesis (referred here as capillary sprouting) is induced primarily by hypoxia, whereas arteriogenesis (referred here as the rapid enlargement of pre-existing collateral arteries, induced by vascular occlusion) is mainly driven by fluid shear stress. Arteriogenesis allows conductance of much larger volumes of blood per unit of time than does the increase in capillary density during angiogenesis. Notwithstanding these major differences, angiogenesis and arteriogenesis share a number of underlying mechanisms, e.g. the involvement of growth factor signalling. This chapter highlights the cellular and molecular events driving the two processes and discusses the therapeutic potential of targeting angiogenesis in cancer and arteriogenesis in cardiovascular diseases.
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25

Allen, Richard D. M., and Henry C. C. Pleass. Donor and recipient kidney transplantation surgery. Edited by Jeremy R. Chapman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0278_update_001.

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Kidney transplant surgery is for thinking surgeons who enjoy being part of a multidisciplinary transplant team. Good ones recognize the small margin for error and avoid difficulties by careful preparation and anticipation of potential pitfalls. Progressively, their role has gained in significance and is now the most important variable in kidney graft loss in the first 6 months after transplantation. Deceased organ donation is complex, expensive, and insufficient in numbers to meet the demand for kidney transplantation. Living donor surgery is therefore a procedure of necessity. Laparoscopic approaches have obvious benefits to the patient but are not operations for the beginner. There are few remaining stalwarts of the open nephrectomy procedure. Because of the limited length of the donor ureter, kidney transplant procedures involve placement of the donor kidney into a heterotopic position with vascular anastomoses to the iliac vessels. No two procedures are the same. Observation of the transplanted kidney changing from a flaccid and pale appearance to one that is firm and pink, and within seconds of removing vascular clamps, is an unforgettable experience for the first timer. Even better is the sight of urine, minutes later. Good transplant centres select their new surgeons carefully!
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Nagpal, Ameet, and Brad Wisler. Thoracic Spinal Stenosis. Edited by Mehul J. Desai. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199350940.003.0011.

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Thoracic spinal stenosis is an uncommon pathologic condition of the spine. This chapter reviews its etiology, epidemiology, anatomic features, symptoms, diagnosis, and treatment. Four of the main causes of thoracic spinal stenosis are ossification of the ligamentum flavum, ossification of the posterior longitudinal ligament, thoracic disc herniation, and thoracic spondylosis. Even rarer secondary causes include generalized skeletal disorders, metabolic and endocrine disorders of the spine, neoplastic lesions, and vascular malformations. The chapter presents a brief review of the currently available surgical techniques. An updated review is provided of the literature on non-surgical management of the disease, mainly interventional pain management.
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27

Jonna, Harsha R., and Michael D. Katz. Use of a Peel-Away Sheath as a Method to Exchange a Clogged Drainage Tube. Edited by S. Lowell Kahn, Bulent Arslan, and Abdulrahman Masrani. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199986071.003.0102.

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There are many methods of exchanging occluded or clogged percutaneous catheters. Typically, catheter exchange is simply performed over a guidewire. When debris occluding the lumen is compact, chronic, or extensive, such exchanges are difficult. Because salvaging an obstructed catheter, without risking loss of access, is difficult, multiple techniques to preserve organ access have been developed. This chapter describes a technique whereby a peel-away sheath is advanced over the catheter to re-establish organ access and facilitate catheter exchange. The placement of a coaxial peel-away sheath is useful for exchanging occluded enteric catheters, biliary drains, abscess drains, nephrostomies, and even selected vascular catheters.
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28

Doumas, Michael, and Chrysoula Boutari. Erectile dysfunction: definition and size of the problem. Edited by Charalambos Vlachopoulos. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0243.

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Erectile dysfunction is currently considered a manifestation of vascular disease in the majority of cases. It is therefore of no surprise that erectile dysfunction is commonly found in patients with overt cardiovascular disease and/or cardiovascular risk factors. Indeed, more than 50% of patients with stable coronary artery disease or acute coronary syndromes suffer from erectile dysfunction, while the prevalence of erectile dysfunction in patients with heart failure is even higher. Likewise, erectile dysfunction is frequently encountered in patients with arterial hypertension, diabetes mellitus, obesity, and dyslipidaemia, as well as in smokers. The increased prevalence of erectile dysfunction in patients with heart disease mandates the active inquiry of this clinical entity in our patients.
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29

Graham, Andrew. Neurological dementias. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199644957.003.0037.

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Dementia in old age is usually due to Alzheimer’s disease, cerebrovascular disease, or mixed pathology. Dementia due to other neurological disorders is uncommon, but important to recognise because management may be very different to that in primary or vascular dementia. This chapter surveys five neurological conditions that may present with dementia in later life: idiopathic normal pressure hydrocephalus (INPH); Huntington’s disease (HD); multiple sclerosis (MS); autoimmune limbic encephalitis (LE); and prion disease. For each disorder the epidemiology, clinical features, investigations & treatment are reviewed, with examples of the characteristic brain imaging changes. Accurate diagnosis of these conditions can be challenging even for physicians with a special interest in dementia, and often requires a neurological referral.
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30

Plotnik, Adam N., and Stephen Kee. Using a Glidewire Cheater and Flow Switch to Temporarily Secure Purse-String Sutures. Edited by S. Lowell Kahn, Bulent Arslan, and Abdulrahman Masrani. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199986071.003.0052.

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Following completion of an arteriovenous graft or fistula intervention, various methods exist by which an interventionalist may achieve hemostasis. Manual compression is the simplest technique but often requires an extended period of time. Many interventionalists will place purse-string sutures at the site of vascular access to achieve hemostasis, with the sutures left in place when the patient leaves the angiography suite. Consequently, these sutures may stay in for an extended period of time and even be present at follow-up interventions many months later or, worse, may get infected. The glidewire cheater and flow switch technique is a method by which hemostasis can be achieved, and it obviates the need for the sutures to be left in place after the patient leaves the angiography suite.
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31

Pipitone, Nicolò, Annibale Versari, and Carlo Salvarani. Large-vessel vasculitis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0133.

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Large-vessel vasculitis includes giant cell arteritis (GCA) and Takayasu's arteritis (TAK). GCA affects patients aged over 50, mainly of white European ethnicity. GCA occurs together with polymyalgia rheumatica (PMR) more frequently than expected by chance. In both conditions, females are affected two to three times more often than males. GCA mainly involves large- and medium-sized arteries, particularly the branches of the proximal aorta including the temporal arteries. Vasculitic involvement results in the typical manifestations of GCA including temporal headache, jaw claudication, and visual loss. A systemic inflammatory response and a marked response to glucocorticoids is characteristic of GCA. GCA usually remits within 6 months to 2 years from disease onset. However, some patients have a chronic-relapsing course and may require long-standing treatment. Mortality is not increased, but there is significant morbidity mainly related to chronic glucocorticoid use and cranial ischaemic events, especially visual loss. The diagnosis of GCA rests on the characteristic clinical features and raised inflammatory markers, but temporal artery biopsy remains the gold standard to support the clinical suspicion. Imaging techniques are also used to demonstrate large-vessel involvement in GCA. Glucocorticoids are the mainstay of treatment for GCA, but other therapeutic approaches have been proposed and novel ones are being developed. TAK mainly involves the aorta and its main branches. Women are particularly affected with a female:male ratio of 9:1. In most patients, age of onset is between 20 and 30 years. Early manifestations of TAK are non-specific and include constitutional and musculoskeletal symptoms. Later on, vascular complications become manifest. Most patients develop vessel stenoses, particularly in the branches of the aortic artery, leading to manifestations of vascular hypoperfusion. Aneurysms occur in a minority of cases. There are no specific laboratory tests to diagnose TAK, although most patients have raised inflammatory markers, therefore, imaging techniques are required to secure the diagnosis. Glucocorticoids are the mainstay of treatment of TAK. However, many patients have an insufficient response to glucocorticoids alone, or relapse when they are tapered or discontinued. Immunosuppressive agents and, in refractory cases, biological drugs can often attain disease control and prevent vascular complications. Revascularization procedures are required in patients with severe established stenoses or occlusions.
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32

Pipitone, Nicolò, Annibale Versari, and Carlo Salvarani. Large-vessel vasculitis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0133_update_003.

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Large-vessel vasculitis includes giant cell arteritis (GCA) and Takayasu’s arteritis (TAK). GCA affects patients aged over 50, mainly of white European ethnicity. GCA occurs together with polymyalgia rheumatica (PMR) more frequently than expected by chance. In both conditions, females are affected two to three times more often than males. GCA mainly involves large- and medium-sized arteries, particularly the branches of the proximal aorta including the temporal arteries. Vasculitic involvement results in the typical manifestations of GCA including temporal headache, jaw claudication, and visual loss. A systemic inflammatory response and a marked response to glucocorticoids is characteristic of GCA. GCA usually remits within 6 months to 2 years from disease onset. However, some patients have a chronic-relapsing course and may require longstanding treatment. Mortality is not increased, but there is significant morbidity mainly related to chronic glucocorticoid use and cranial ischaemic events, especially visual loss. The diagnosis of GCA rests on the characteristic clinical features and raised inflammatory markers, but temporal artery biopsy remains the gold standard to support the clinical suspicion. Imaging techniques are also used to demonstrate large-vessel involvement in GCA. Glucocorticoids are the mainstay of treatment for GCA, but other therapeutic approaches have been proposed and novel ones are being developed. TAK mainly involves the aorta and its main branches. Women are particularly affected with a female:male ratio of 9:1. In most patients, age of onset is between 20 and 30 years. Early manifestations of TAK are non-specific and include constitutional and musculoskeletal symptoms. Later on, vascular complications become manifest. Most patients develop vessel stenoses, particularly in the branches of the aortic artery, leading to manifestations of vascular hypoperfusion. Aneurysms occur in a minority of cases. There are no specific laboratory tests to diagnose TAK, although most patients have raised inflammatory markers, therefore, imaging techniques are required to secure the diagnosis. Glucocorticoids are the mainstay of treatment of TAK. However, many patients have an insufficient response to glucocorticoids alone, or relapse when they are tapered or discontinued. Immunosuppressive agents and, in refractory cases, biological drugs can often attain disease control and prevent vascular complications. Revascularization procedures are required in patients with severe established stenoses or occlusions.
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33

Reinecke, Holger. Epidemiology and global burden of peripheral arterial disease and aortic aneurysms. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0068.

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Peripheral artery disease (PAD) and aortic aneurysms are common diseases which show an increasing prevalence and incidence. From community-based trials assessing ankle–brachial indices, 2–4% of the general population have been shown to be affected by PAD, which increases up to 15% in those above 70 years of age. About 30–40% of the in-hospital cases with PAD have critical limb ischaemia and suffer from a 1-year mortality of 20–40%. Abdominal aortic aneurysms (AAAs) also show a relatively high prevalence of about 1–2% in the general population as found by large-scale, systematic duplex screening. Of these, about 5% come to hospital admittance with a ruptured AAA which is still associated with an in-hospital mortality of up to 50%. The prevalence of thoracic aortic aneurysms (TAAs) was reported to be at about 0.16–0.34% in selected subgroups of the general population. The incident cases of TAAs have risen from 10/100,000 cases in the late 1980s up to about 17/100,000 cases in the first decade of this millennium. It is noteworthy that PAD and aortic aneurysms as well as their associated co-morbidities remain in many cases underdiagnosed and undertreated. This leads to a high cardiovascular morbidity and mortality which could not be obviously markedly reduced in the recent decades. Since nearly all vascular disorders are systemic diseases, not only the specific vessel bed which leads to a presentation should be assessed but also all other possible vascular manifestations should be thoroughly examined to reduce adverse events.
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34

Hayhow, Bradleigh, and Sergio Starkstein. Biological Effects of Depression. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190603342.003.0005.

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This chapter examines the bidirectional relationship between depression and stroke. It is now clearly established that depression is a significant risk factor for stroke, and vice-versa. We review the main biological and demographic factors underlying the association between stroke and depression, the predicted mortality, the mechanism of post-stroke depression, and recent findings on its pharmacological prevention. We conclude by stressing the need for developing effective strategies to manage the burden of illness associated with these interacting conditions. As with the cardiovascular system depression has major effects on the occurrence of stroke. Morbidity and mortality are increased for patients with cerebral vascular accidents (CVA) who are depressed and is seen even in a 10-year follow-up. Depression should be treated concurrently with the management of the acute phase of a CVA.
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35

Eyre, Lorna, and Simon Whiteley. In-hospital transfer of the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0004.

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While focus has traditionally been on the planning, logistics, and outcome of inter-hospital transfers of the critically-ill patient, attention is turning to in-hospital transfers. Numerically, more in-hospital transfers occur and there is growing evidence that these are associated with a high incidence of adverse events, and increased morbidity and mortality. Appropriate planning, communication, and preparation are essential. Patients should be resuscitated and stabilized (optimized) prior to transfer, to prevent deterioration or instability during transfer. Endotracheal tubes and vascular access devices should be secure. The minimum recommended standards of monitoring should be applied. All drugs and equipment likely to be required during the transfer should be checked and available. Critically-ill patients should be accompanied by personnel with the appropriate knowledge skills and experience to carry out the transfer safely and to deal with any complications or incidents that arise.
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36

Patarroyo, Sully Xiomara Fuentes, and Craig Anderson. Management of ischaemic stroke. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0236.

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Ischaemic stroke is the most common cause of stroke around the world. It is a complex disease with a range of causes, manifestations, outcomes, and treatments. As the therapeutic time window to rescue or ‘protect’ the brain from ischaemic damage is extremely short, effective treatment requires coordinated systems of care, which commence in the prehospital paramedical setting and continue through the emergency department into the critical care environment, neurology ward, rehabilitation, and re-settlement back home. Successful outcomes from ischaemic stroke can be achieved through the effective use of thrombolytic therapy to re-canalize an occluded vessel and re-perfuse the ‘at risk’ area of the brain. Other aspects of management include the prevention of complications of the neurological (cerebral) disability, timely introduction of rehabilitation, realistic goal-setting towards satisfactory recovery, and secondary prevention measures to reduce the high risk of recurrent stroke and other serious vascular events.
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37

Tatlisumak, Turgut, and Lars Thomassen, eds. Ischaemic Stroke in the Young. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198722366.001.0001.

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Stroke in the young is different, complex, and challenging. This book delivers a comprehensive review of the different aspects of young ischaemic stroke. Incidence, risk factors, and aetiology differ notably from those seen in the elderly. There is an increased prevalence of traditional risk factors already at a young age, but the book also focuses on special risk factors in young stroke patients. In many young stroke patients, aetiology remains unclear. The book outlines an extensive diagnostic workup and a stroke subtype classification adapted for young strokes. Gender differences are prevalent in young stroke. The book describes risk factors that are either unique or more prevalent in women and the importance of treating them aggressively. Stroke symptoms in children are comparable to those in adults, but there is a dramatic bystander delay in diagnosing the stroke. The text therefore also deals with rapid stroke recognition and adaption to the special needs in children. Young stroke patients are under-represented in randomized controlled treatment trials. In the emergency setting, unusual clinical findings and off-label situations may be faced and the decision-making process may be challenging. Recommendations for secondary prevention are also mainly extrapolated from studies in older individuals. The authors extrapolate data and draw conclusions on the acute and prophylactic treatment of young stroke. Prognosis after young stroke is poor. Even minor stroke may have devastating life-long consequences for quality of life, education, and working capacity. The book points to the opportunity for lifelong prevention of vascular events.
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38

Williams, Erin S. Pulmonary Hypertension. Edited by Erin S. Williams, Olutoyin A. Olutoye, Catherine P. Seipel, and Titilopemi A. O. Aina. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190678333.003.0029.

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Pulmonary hypertension is one of the most challenging medical conditions for even the most experienced anesthesiologist to manage. The very dynamic nature of pulmonary vascular disease lends itself to potential catastrophic changes that can increase the perioperative morbidity and mortality. Given the potential for significant hemodynamic, oxygenation, and ventilation changes during perioperative care it is imperative that the pediatric anesthesiologist not only perform a history and physical exam in this high-risk patient population but also carefully evaluate the most recent cardiac studies such as echocardiograms and catheterizations. The anesthesiologist must ensure that the patient is not overdue for cardiology exams and studies. Finally, the pediatric anesthesiologist must also communicate with the surgeon and cardiologist regarding the risk and benefit of the procedure; along with the severity of the patient’s pulmonary hypertension, in order to formulate and ultimately execute an anesthetic plan that decreases the possibility for perioperative complications.
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39

Metzner, Julia I., and Deepak Sharma. Venous Air Embolism. Edited by David E. Traul and Irene P. Osborn. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190850036.003.0025.

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Venous air embolism (VAE) is typically the entrainment of air from the surgical field into the vascular system producing adverse systemic effects based on the severity of embolism. Historically, VAE has most often been associated with sitting position craniotomies. However, there is now a clear recognition of the potential risk of this complication during craniotomy in any position, albeit with lesser incidence and severity. VAE can also occur during cervical spine surgery in the sitting position, although less often. While in many circumstances VAE may be subclinical and even undetected, it has the potential to lead to significant cardiovascular compromise during surgery, with the risk of adverse outcomes. Hence, it is imperative for anesthesiologists to be aware of the causes of and risk factors for VAE, its clinical presentation, diagnostic options, and treatment strategies to effectively prevent and intervene early in this potentially fatal condition.
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40

Madl, Ulrike. Pathophysiology of glucose control. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0258.

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Hyperglycaemia is a frequent phenomenon in critically-ill patients, associated with increased morbidity and mortality. Hyperglycaemia results in cellular glucose overload and toxic adverse effects of glycolysis and oxidative phosphorylation, especially in tissues with insulin-independent glucose uptake, and acute hyperglycaemia can exert a variety of negative effects. It is the main side effect of intensive insulin therapy. Both severe and moderate hypoglycaemia are independent risk factors of mortality in critically-ill patients. Prolonged hypoglycaemia induces neuronal damage, but may also have adverse cardiovascular effects. Several risk factors predispose critically-ill patients to hypoglycaemic events. Rapid glucose fluctuations may induce oxidative stress and lead to vascular damage. Glucose complexity is a marker of endogenous glucose regulation. Association between hyperglycaemia and outcome is weaker in diabetic critically-ill patients than in non-diabetic patients. Pre-admission glucose control in diabetic critically-ill patients plays a role in the response to glucose control and mortality.
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41

Kotseva, Kornelia, Neil Oldridge, and Massimo F. Piepoli. Evaluation of preventive cardiology. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656653.003.0026.

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The Joint European Societies guidelines on cardiovascular disease (CVD) prevention define lifestyle and risk factor targets for patients with coronary or other atherosclerotic disease and people at high risk of developing CVD. However, several surveys in Europe and the United States showed inadequate lifestyle and risk factor management and under-use of prophylactic drug therapies in primary and secondary CVD prevention. Various professional associations have developed core components, standards, and outcome measures to evaluate quality of care and provide guidelines for identifying opportunities for improvements. Optimal control of cardiovascular risk factors is one of the most effective methods for reducing vascular events in patients with atherosclerotic disease or high cardiovascular risk. Improving treatment adherence is also very important. Health-related quality of life (HRQL) is considered as an outcome measure in research studies and in clinical practice. HRQL measures can help in improving patient-clinician communication, screening, monitoring, and continuous assessment of quality of care.
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42

Kotseva, Kornelia, Neil Oldridge, and Massimo F. Piepoli. Evaluation of preventive cardiology. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199656653.003.0026_update_001.

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The Joint European Societies guidelines on cardiovascular disease (CVD) prevention define lifestyle and risk factor targets for patients with coronary or other atherosclerotic disease and people at high risk of developing CVD. However, several surveys in Europe and the United States showed inadequate lifestyle and risk factor management and under-use of prophylactic drug therapies in primary and secondary CVD prevention. Various professional associations have developed core components, standards, and outcome measures to evaluate quality of care and provide guidelines for identifying opportunities for improvements. Optimal control of cardiovascular risk factors is one of the most effective methods for reducing vascular events in patients with atherosclerotic disease or high cardiovascular risk. Improving treatment adherence is also very important. Health-related quality of life (HRQL) is considered as an outcome measure in research studies and in clinical practice. HRQL measures can help in improving patient-clinician communication, screening, monitoring, and continuous assessment of quality of care.
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43

Becker, Richard C., and Frederick A. Spencer. Fibrinolytic and Antithrombotic Therapy. Oxford University Press, 2006. http://dx.doi.org/10.1093/oso/9780195155648.001.0001.

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Thrombotic disorders of the circulatory system represent the leading cause of morbidity, motality, and health care expenditure in the United States. Fibrinolytic and Antithrombotic Therapy provides a practical, evidence-based approach to the management of thrombotic disorders for all clinicians involved in the care of patients with these disorders. It provides not only vital conceptual information on fibrinolytic and antithrombotic therapy, but also the means to apply it to everyday decision making and patient care. Focusing on managment guidelines and critical pathways, the text stresses practicality and usability. It will be a valuable resource for the wide range of clinicians involved in the care of patients with these disorders, including cardiologists, emergency physicians, primary care physicians, hematologists, neurologists, intensivists, pharmacists, and nurse practitioners. The origins of mammalian blood coagulation can be traced back over 400 million years. Despite its long history, it is only within the past century that this complex and pivotal teleologic system has begun to be understood. Most recently, the intricacies of hemostasis and pahtologic thrombosis have come to light, leading the way toward new, more effective, and safer treatment modalities. The Second Edition of Fibrinolytic and Antithrombotic Therapy, even more concise and clinically relevant than the First, provides vital, evidence-based information on management of patients with arterial and venous thrombotic disorders. Since the First Edition, the text has been expanded to cover the evolving topics of atherothrombosis, thrombocardiology, hematologic/thrombophilic conditions, and vascular medicine. It includes up-to-date guidelines for antithrombotic and fibrinolytic therapy, and offers concise summaries of current "standards of care." Chapters are dedicated to discussions of patient-specific therapeutics and to the importance of genomics, proteomics, and metabolomics in defining genotype-phenotype relationships, while throughout the book coagulation, inflammation, and vascular medicine are newly examined as elements in an intricatley-linked triad of biochemical and cellular based phenomenology.
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Radermacher, Peter, and Claus-Martin Muth. Pathophysiology and management of depth-related disorders. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0351.

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Decompression illness comprises decompression sickness resulting from tissue inert gas super-saturation and pulmonary barotraumas due to alveolar or airway over-distension. Gas bubbles can cause vascular obstruction or tissue compression, resulting in tissue ischaemia and oedema. Interactions between the blood–gas interface and the endothelium will result in further tissue damage, and trigger an inflammatory cascade with capillary leakage and haemoconcentration. Decompression illness may mimic any other emergency pathology and any emergency coinciding with decompression is ‘due to’ decompression. Pulmonary barotrauma-induced arterial gas embolism and decompression sickness can be discriminated according to the onset of symptoms, with gas embolism predominantly developing within a few minutes after or even during decompression. Specific treatment consists of hyperbaric oxygen treatment, using several empirically-derived hyperbaric oxygen treatment schedules. Currently, there is no recognized pharmacological treatment, but fluid resuscitation is useful to counteract haemoconcentration and dehydration. Early treatment initiation is mandatory, and certain technical issues must be considered for the management of critically-ill patients in a hyperbaric chamber.
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45

Giuseffi, Jennifer, John McPherson, Chad Wagner, and E. Wesley Ely. Acute cognitive disorders: recognition and management of delirium in the cardiovascular intensive care unit. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0074.

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Delirium is the most common acute cognitive disorder seen in critically ill patients in the cardiovascular intensive care unit. It is defined as a disturbance of consciousness and cognition that develops suddenly and fluctuates over time. Delirious patients can become hyperactive, hypoactive, or both. The occurrence of delirium during hospitalization is associated with increased in-hospital and long-term morbidity and mortality. The cause of delirium is multifactorial and may include imbalances in neurotransmitters, inflammatory mediators, metabolic disturbances, impaired sleep, and the use of sedatives and analgesics. Patients with advanced age, dementia, chronic illness, extensive vascular disease, and low cardiac output are at particular risk of developing delirium. Specialized bedside assessment tools are now available to rapidly diagnose delirium, even in mechanically ventilated patients. Increased awareness of delirium risk factors, in addition to non-pharmacological and pharmacological treatments for delirium, can be effective in reducing the incidence of delirium in cardiac patients and in minimizing adverse outcomes, once delirium occurs.
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46

McPherson, John, Jennifer Giuseffi, Chad Wagner, and E. Wesley Ely. Acute cognitive disorders: recognition and management of delirium in the cardiovascular intensive care unit. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199687039.003.0074_update_001.

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Delirium is the most common acute cognitive disorder seen in critically ill patients in the cardiovascular intensive care unit. It is defined as a disturbance of consciousness and cognition that develops suddenly and fluctuates over time. Delirious patients can become hyperactive, hypoactive, or both. The occurrence of delirium during hospitalization is associated with increased in-hospital and long-term morbidity and mortality. The cause of delirium is multifactorial and may include imbalances in neurotransmitters, inflammatory mediators, metabolic disturbances, impaired sleep, and the use of sedatives and analgesics. Patients with advanced age, dementia, chronic illness, extensive vascular disease, and low cardiac output are at particular risk of developing delirium. Specialized bedside assessment tools are now available to rapidly diagnose delirium, even in mechanically ventilated patients. Increased awareness of delirium risk factors, in addition to non-pharmacological and pharmacological treatments for delirium, can be effective in reducing the incidence of delirium in cardiac patients and in minimizing adverse outcomes, once delirium occurs.
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47

Banerjee, Amitava, and Kaleab Asrress. Screening for cardiovascular disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0351.

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Screening involves testing asymptomatic individuals who have risk factors, or individuals who are in the early stages of a disease, in order to decide whether further investigation, clinical intervention, or treatment is warranted. Therefore, screening is classically a primary prevention strategy which aims to capture disease early in its course, but it can also involve secondary prevention in individuals with established disease. In the words of Geoffrey Rose, screening is a ‘population’ strategy. Examples of screening programmes are blood pressure monitoring in primary care to screen for hypertension, and ultrasound examination to screen for abdominal aortic aneurysm. The effectiveness and feasibility of screening are influenced by several factors. First, the diagnostic accuracy of the screening test in question is crucial. For example, exercise ECG testing, although widely used, is not recommended in investigation of chest pain in current National Institute for Health and Care Excellence guidelines, due to its low sensitivity and specificity in the detection of coronary artery disease. Moreover, exercise ECG testing has even lower diagnostic accuracy in asymptomatic patients with coronary artery disease. Second, physical and financial resources influence the decision to screen. For example, the cost and the effectiveness of CT coronary angiography and other new imaging modalities to assess coronary vasculature must be weighed against the cost of existing investigations (e.g. coronary angiography) and the need for new equipment and staff training and recruitment. Finally, the safety of the investigation is an important factor, and patient preferences and physician preferences should be taken into consideration. However, while non-invasive screening examinations are preferable from the point of view of patients and clinicians, sometimes invasive screening tests may be required at a later stage in order to give a definitive diagnosis (e.g. pressure wire studies to measure fractional flow reserve in a coronary artery). The WHO’s principles of screening, first formulated in 1968, are still very relevant today. Decision analysis has led to ‘pathways’ which guide investigation and treatment within screening programmes. There is increasing recognition that there are shared risk factors and shared preventive and treatment strategies for vascular disease, regardless of arterial territory. The concept of ‘vascular medicine’ has gained credence, leading to opportunistic screening in other vascular territories if an individual presents with disease in one territory. For example, post-myocardial infarction patients have higher incidence of cerebrovascular and peripheral arterial disease, so carotid duplex scanning and measurement of the ankle–brachial pressure index may be valid screening approaches for arterial disease in other territories.
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48

Immani, Sudhir, and John Loughrey. Ultrasound. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198713333.003.0054.

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The use of ultrasound in obstetric anaesthesia practice has accelerated in the past decade, following a typical pattern of a small number of enthusiastic early adopters, to a current phase of more widespread use. The use of ultrasound in everyday practice has yet to include the majority of practitioners. However, more widespread availability of equipment and also training opportunities will ensure that it may be a future standard in obstetric units. The most obvious and current application for ultrasound for obstetric anaesthetists is in the improvement of the safety, quality, and success of neuraxial anaesthesia. This chapter sets out a description of current technique and knowledge of this application of ultrasound by obstetric anaesthetists and will give the reader a good overview of this topic. There are other applications of ultrasound in obstetric anaesthesia practice including vascular access, cardiac assessment in patients with cardiovascular collapse, and possibly even gastric volume assessment. Future equipment modifications may enhance the technique with smaller ultrasound probes for more accurate skin marking and also with enhanced image quality.
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49

Whittle, Ian. Raised intracranial pressure, cerebral oedema, and hydrocephalus. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0604.

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The brain is protected by the cranial skeleton. Within the intracranial compartment are also cerebrospinal fluid, CSF, and the blood contained within the brain vessels. These intracranial components are in dynamic equilibrium due to the pulsations of the heart and the respiratory regulated return of venous blood from the brain. Normally the mean arterial blood pressure, systemic venous pressure, and brain volume are regulated to maintain physiological values for intracranial pressure, ICP. There are a range of very common disorders such as stroke, and much less common, such as idiopathic intracranial hypertension, that are associated with major disturbances of intracranial pressure dynamics. In some of these the contribution to pathophysiology is relatively minor whereas in others it may be substantial and be a major contributory factor to morbidity or even death.Intracranial pressure can be disordered because of brain oedema, disturbances in CSF flow, mass lesions, and vascular engorgement of the brain. Each of these may have variable causes and there may be interactions between mechanisms. In this chapter the normal regulation of intracranial pressure is outlined and some common disease states in clinical neurological practice that are characterized by either primary or secondary problems in intracranial pressure dynamics described.
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Magder, Sheldon. Central venous pressure monitoring in the ICU. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0132.

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Abstract:
Central venous pressure (CVP) is at the crucial intersection of the force returning blood to the heart and the force produced by cardiac function, which drives the blood back to the systemic circulation. The normal range of CVP is small so that before using it one must ensure proper measurement, specifically the reference level. A useful approach to hypotension is to first determine if arterial pressure is low because of a decrease in vascular resistance or a decrease in cardiac output. This is done by either measuring cardiac output or making a clinical assessment blood flow. If the cardiac output is decreased, next determine whether this is because of a cardiac pump problem or a return problem. It is at this stage that the CVP is most helpful for these options can be separated by considering the actual CVP or even better, how it changed with the change in cardiac output. A high CVP is indicative of a primary pump problem, and a low CVP and return problem. Understanding the factors that determine CVP magnitude, mechanisms that produce the components of the CVP wave form and changes in CVP with respiratory efforts can also provide useful clinical information. In many patients, CVP can be estimated on physical exam.
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