Books: 'Vascular injury'

1

Simon, Daniel I., and Campbell Rogers. Vascular Disease and Injury. New Jersey: Humana Press, 2000. http://dx.doi.org/10.1385/1592590039.

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2

Love, Graham P. Endothelin-I as a mediator of injury in vascular endothelial cells. Dublin: University College Dublin, 1997.

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3

Brace, Sarah. A guide to ozone injury in vascular plants of the Pacific Northwest. Portland, Or. (333 S.W. First Avenue, P.O. Box 3890 Portland, 97208-3890): U.S. Department of Agriculture, Forest Service, Pacific Nortwest Research Station, 1999.

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4

The clinical neuropsychiatry of stroke: Cognitive, behavioral, and emotional disorders following vascular brain injury. Cambridge: Cambridge University Press, 1998.

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5

V, Schaff Hartzell, ed. Vasoactive factors produced by the endothelium: Physiology and surgical implications. Austin: R.G. Landes, 1994.

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6

Kim, Tony Tae Yub. Vascular growth after balloon catheter injury in normal rats treated with high fat diet and insulin implants. Ottawa: National Library of Canada, 2002.

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7

Vascular Disease And Injury. Humana Press, 2010.

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8

Vascular endothelium: Responses to injury. New York: Plenum Press, 1996.

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9

John D. Catravas Allan D. Callow. Vascular Endothelium: Responses to Injury. Brand: Springer, 2011.

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10

Ryan, Una S., Allan D. Callow, and John D. Catravas. Vascular Endothelium: Responses to Injury. Springer, 2012.

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11

Vascular Endothelium: Responses to Injury. Springer, 2014.

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12

(Editor), Allan D. Callow, John D. Catravas (Editor), and Una S. Ryan (Editor), eds. Vascular Endothelium: Responses to Injury. Springer, 1996.

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13

Rogers, Campbell, and Daniel I. Simon. Vascular Disease and Injury: Preclinical Research. Humana Press, 2000.

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14

1953-, Johnson Arnold, and Ferro Thomas J. 1956-, eds. Lung vascular injury: Molecular and cellular response. New York: Marcel Dekker, 1992.

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15

Warwick, David, Roderick Dunn, Erman Melikyan, and Jane Vadher. Vascular. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199227235.003.0018.

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Vascular anatomy 592Vascular assessment 600Hand–arm vibration syndrome (Vibration white finger) 604Vascular anomalies 606Acute vascular injury 612Occlusion 614Raynaud's disease 617Compartment syndrome 618• This is divided into three parts by the scalenus anterior muscle (this lies over the 2nd part)....

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16

Iatrogenic Vascular Injury: A Discourse on Surgical Technique. Futura Pub Co, 1990.

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17

J, Bunt T., ed. Iatrogenic vascular injury: A discourse on surgical technique. Mount Kisco, NY: Futura Pub. Co., 1990.

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18

Han, Jing-Yan, Qiaobing Huang, Jincai Luo, and Gerald A. Meininger, eds. Traditional Chinese Medicine: Organ Vascular Injury - Volume II. Frontiers Media SA, 2021. http://dx.doi.org/10.3389/978-2-88971-142-0.

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19

(Editor), Daniel I. Simon, and Campbell Rogers (Editor), eds. Vascular Disease and Injury: Preclinical Research (Contemporary Cardiology). Humana Press, 2001.

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20

Sierakowski, Adam, David Warwick, and Roderick Dunn. Vascular. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198757689.003.0018.

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Vascular pathology in the hand may present to many different specialties, and delayed referral to hand specialists is not unusual. We provide an overview of vascular hand anatomy and pathophysiology to enable early diagnosis and treatment. We discuss general assessment of vascular hand pathology, including vascular anomalies, vascular injury, and Raynaud’s disease. It is important to understand the diagnosis and emergency surgical treatment of compartment syndrome of the upper limb which if unrecognized can lead to permanent loss of function from post-ischaemic fibrosis (and may be less anticipated than lower limb compartment syndrome).

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21

Huang, Yuli, Zhen Yang, and Ji Bihl, eds. Cardiovascular Risk Factors: Related Vascular Injury and New Molecular Biomarkers. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-83250-313-3.

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22

Chaloner, E. Combined vascular and orthopaedic injuries. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199550647.003.012009.

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♦ Early diagnosis of an arterial injury is critical in reducing the risk of limb loss♦ Don’t assume that missing pulses are due to arterial ‘spasm’♦ Don’t assume that presence of distal pulses rules out a proximal vascular injury – arterial intimal tears can occlude the vessel many hours after the initial injury♦ After an arterial repair has been completed there is still a risk of subsequent compartment syndrome from reperfusion♦ Arterial shunts can procure some time for skeletal fixation prior to definitive arterial repair or grafting.

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23

Chatterjee, Shampa, Silvia Lacchini, Wolfgang Jungraithmayr, and Felix W. Wehrli, eds. Vascular Health: The Endothelial Perspective in Regulation of Inflammation and Injury. Frontiers Media SA, 2021. http://dx.doi.org/10.3389/978-2-88971-418-6.

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24

Kamisah, Yusof, Zakiah Jubri, Mas Rizky A. A. Syamsunarno, and Yue Liu, eds. Medicinal Plants in the Treatment of Myocardial Injury and Vascular Diseases. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88974-999-7.

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25

Kamisah, Yusof, Zakiah Jubri, Mas Rizky A. A. Syamsunarno, and Yue Liu, eds. Medicinal Plants in the Treatment of Myocardial Injury and Vascular Diseases. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88974-999-7.

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26

Karamchandani, Rahul, and Nancy R. Barbas. Vascular Cognitive Impairment. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0021.

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Vascular cognitive impairment (VCI) refers to the spectrum of cognitive disturbances that result from cerebrovascular brain injury. Cerebrovascular disease is associated with multiple underlying pathologies. Risk factors, clinical features, and treatment options overlap with those associated with Alzheimer’s disease, another common cause of cognitive decline. The complexity of vascular cognitive impairment and, notably, the interplay between clinical, pathologic, genetic, and biomarker characteristics of VCI and Alzheimer’s disease are discussed. The chapter places an emphasis on vascular cognitive impairment resulting from disease affecting small vessels, in contrast to that due to disease involving large vessels, in an effort to focus on a large body of evolving work and ongoing attempts at improving understanding of this complex entity.

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27

Thornton, Clare, and Justin Mason. Vascular biology. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0057.

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Vascular biology is the study of the physiology of the vasculature and how it may be the target for disease processes. An understanding of vascular biology is central to the study of rheumatic disease for three reasons: it is an integral part of a functioning immune system; it is the primary site of pathology in many conditions; and it is the site of the important secondary complications of chronic inflammation, endothelial dysfunction and atherosclerosis. Vascular biology requires a detailed knowledge of the anatomy and physiology of the vasculature and its constituent vessels. The multistep process by which leucocytes interact with endothelium lining postcapillary venules in order to leave the circulation and migrate towards a site of inflammation is central to the pathology of inflammatory disease. The vasculature is the primary site of injury in several rheumatic diseases, including the vasculitides. It may also be damaged by chronic inflammation, leading to endothelial dysfunction and accelerated atherosclerosis. Thrombosis is also a critical pathological process in several chronic inflammatory diseases, particularly the anti-phospholipid antibody syndrome and Behçet's syndrome. The vascular endothelium is central to angiogenesis, the process of new capillary outgrowth, upon which synovial proliferation in inflammatory arthritis is dependent. Angiogenesis is inhibited by current anti-rheumatic therapies and may become a target for novel anti-rheumatic drugs. An increasing area of research concerns the direct effects of drugs used in the treatment of atherosclerosis and inflammatory disease on the endothelium, and whether these agents are beneficial or harmful. Of particular interest to rheumatologists are the vascular effects of statins, disease-modifying anti-rheumatic drugs (DMARDs), immunosuppressants, and cyclooxygenase inhibitors.

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28

Thornton, Clare, and Justin Mason. Vascular biology. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199642489.003.0057_update_001.

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Vascular biology is the study of the physiology of the vasculature and how it may be the target for disease processes. An understanding of vascular biology is central to the study of rheumatic disease for three reasons: it is an integral part of a functioning immune system; it is the primary site of pathology in many conditions; and it is the site of the important secondary complications of chronic inflammation, endothelial dysfunction and atherosclerosis. Vascular biology requires a detailed knowledge of the anatomy and physiology of the vasculature and its constituent vessels. The multistep process by which leucocytes interact with endothelium lining postcapillary venules in order to leave the circulation and migrate towards a site of inflammation is central to the pathology of inflammatory disease. The vasculature is the primary site of injury in several rheumatic diseases, including the vasculitides. It may also be damaged by chronic inflammation, leading to endothelial dysfunction and accelerated atherosclerosis. Thrombosis is also a critical pathological process in several chronic inflammatory diseases, particularly the anti-phospholipid antibody syndrome and Behçet’s syndrome. The vascular endothelium is central to angiogenesis, the process of new capillary outgrowth, upon which synovial proliferation in inflammatory arthritis is dependent. Angiogenesis is inhibited by current anti-rheumatic therapies and may become a target for novel anti-rheumatic drugs. An increasing area of research concerns the direct effects of drugs used in the treatment of atherosclerosis and inflammatory disease on the endothelium, and whether these agents are beneficial or harmful. Of particular interest to rheumatologists are the vascular effects of statins, disease-modifying anti-rheumatic drugs (DMARDs), immunosuppressants, and cyclooxygenase inhibitors.

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29

1954-, Peterson David L., Bowers Darci, Pacific Northwest Research Station (Portland, Or.), United States. Forest Service. Pacific Northwest Region, and United States. National Park Service, eds. A Guide to ozone injury in vascular plants of the Pacific Northwest. Portland, Or: U.S. Dept. of Agriculture, Forest Service, Pacific Northwest Research Station, 1999.

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30

Garaffa, Giulio, Salvatore Sansalone, and David J. Ralph. Male genital injury. Edited by David John Ralph. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0109.

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Male genital trauma, a relatively rare condition in the Western world, usually affects young men and encompasses a wide spectrum of injuries, which in the most severe cases may lead to a complete long-term loss of sexual and urinary function. When managing genital trauma, it is paramount to identify possible associated bony, vascular, bowel, and urinary tract injuries, which are present in up to 83% of cases, and should require immediate treatment, as they may be potentially life-threatening. The management of the genital trauma should be deferred to a later stage, when associated injuries have been successfully dealt with and the patient condition is stable. Therefore, a prompt and effective management of genital injuries is paramount to prevent devastating effects on patient’s self-image and quality of life. Classification of genital injuries is extremely complex, as an offending mechanism can lead to a broad spectrum of lesions.

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31

Swanson, Karen L. Neoplastic and Vascular Diseases. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0618.

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Neoplastic and vascular disorders are reviewed. Lung cancer is the most common malignancy and cause of cancer death in both men and women worldwide. The incidence of new lung cancers has continued to decrease in men and increase in women. The risk factors include cigarette smoking, other carcinogens, cocarcinogens, radon exposure, arsenic, asbestos, coal dust, chromium, vinyl chloride, chloromethyl ether, and chronic lung injury. Genetic and nutritional factors have been implicated. Among vascular disorders, pulmonary embolism is most common. Pulmonary embolism (PE) is the cause of death in 5% to 15% of hospitalized patients who die in the United States. In a multicenter study of PE, the mortality rate at 3 months was 15% and important prognostic factors included age older than 70 years, cancer, congestive heart failure, COPD, systolic arterial hypotension, tachypnea, and right ventricular hypokinesis.

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32

Gilani, Ramyar, and Kenneth L. Mattox. Management of vascular injuries. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0335.

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Management of vascular injuries presents a unique set of challenges. Vascular injuries are commonly accompanied by injuries to other organ systems, and affected patients may be critically ill and close to the limits of their physiological reserve. Complications of vascular injury are bleeding, leading to hypovolaemic shock and consumptive coagulopathy, and vascular occlusion causing distal ischaemia and acidosis. When the patient’s clinical condition allows the diagnosis of vascular injuries relies on computerized tomographic angiography or digital subtraction angiography. Control of haemorrhage can be achieved with direct manual pressure, tourniquets for life-threatening extremity haemorrhage, or temporary occlusion with a balloon catheter. Simple surgical repairs may be performed. Ligation is quite well tolerated for arteries of distribution. For patients with significant or ongoing bleeding, a transfusion strategy using a 1:1:1 ratio of packed red blood cells, fresh frozen plasma, and platelets is currently considered the best strategy. For more stable patients, complex and definitive vascular repairs can be considered.

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33

Ho, Bernard. Integrin-linked kinase in the vascular smooth muscle cell response to arterial injury. 2006.

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34

Robinson, Robert G. Clinical Neuropsychiatry of Stroke: Cognitive, Behavioral and Emotional Disorders Following Vascular Brain Injury. Cambridge University Press, 2012.

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35

Robinson, Robert G. Clinical Neuropsychiatry of Stroke: Cognitive, Behavioral and Emotional Disorders Following Vascular Brain Injury. Cambridge University Press, 2006.

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36

Robinson, Robert G. Clinical Neuropsychiatry of Stroke: Cognitive, Behavioral and Emotional Disorders Following Vascular Brain Injury. Cambridge University Press, 2006.

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37

Robinson, Robert G. Clinical Neuropsychiatry of Stroke: Cognitive, Behavioral and Emotional Disorders Following Vascular Brain Injury. Cambridge University Press, 2009.

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38

The Clinical Neuropsychiatry of Stroke: Cognitive, Behavioral and Emotional Disorders following Vascular Brain Injury. 2nd ed. Cambridge University Press, 2006.

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39

Ladner, Travis R., Nishant Ganesh Kumar, Lucy He, and J. Mocco. Neuroprotection for Vascular and Endovascular Neurosurgery. Edited by David L. Reich, Stephan Mayer, and Suzan Uysal. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190280253.003.0019.

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The complexity of neurovascular disease presents a challenge to the surgical and anesthesia teams managing patients with such conditions. With open or endovascular techniques, abrupt changes in hemodynamic status and intracranial pressure are an ever-present concern throughout the perioperative period. Monitoring of neurological status, hemodynamic parameters, and intracranial pressure are important adjuncts. Targeted physiologic and pharmacological interventions are critical to ensuring safe completion of complex procedures and the prevention secondary injury. This chapter reviews common complications of cerebrovascular and endovascular operations and their risk factors and summarize clinical principles, strategies, and considerations for maximizing neuroprotection in the treatment of neurovascular disease.

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40

Coppola, Silvia, and Franco Valenza. Inhalation injury in the ICU. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0107.

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Inhalation injury represents one of the most serious associated injuries complicating the care of thermally-injured patient. It can result in severe respiratory failure and acute respiratory distress syndrome (ARDS) by three mechanisms—thermal or chemical injury, and impairment of systemic oxygen supply. Thermal injury can cause erythema, ulceration, and progressive, life-threatening oedema, particularly of the upper airways. Chemical injury is due to irritants or cytotoxic compounds, and depends on the material burned, the temperature of the fire, and the amount of oxygen present in the fire environment. It is responsible for irritation, ulceration, and oedema of the mucosal surface, and the initiation of a lung inflammatory reaction when small particles reach the alveoli. Moreover, the increased vascular permeability, and the reduced surfactant production carry a significant risk in the development of pneumonia and ARDS. Bronchospasm and upper airway oedema can occur rapidly, while lower airway oedema can be asymptomatic for up to 24 hours. Lung imaging techniques may not reveal injured areas for the first 24–48 hours. Fibre optic bronchoscopy is considered to be the most direct diagnostic method for the definitive diagnosis of inhalation injury. The patient management includes airways assessment, adequate fluid resuscitation, and mechanical ventilation when required. All victims of smoke inhalation should be always evaluated for cyanide and carbon monoxide poisoning.

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41

Goligorsky, Michael S., Julien Maizel, Radovan Vasko, May M. Rabadi, and Brian B. Ratliff. Pathophysiology of acute kidney injury. Edited by Norbert Lameire. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0221.

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In the intricate maze of proposed mechanisms, modifiers, modulators, and sensitizers for acute kidney injury (AKI) and diverse causes inducing it, this chapter focuses on several common and undisputable strands which do exist.Structurally, the loss of the brush border, desquamation of tubular epithelial cells, and obstruction of the tubular lumen are commonly observed, albeit to various degrees. These morphologic hallmarks of AKI are accompanied by functional defects, most consistently reflected in the decreased glomerular filtration rate and variable degree of reduction in renal blood flow, accompanied by changes in the microcirculation. Although all renal resident cells participate in AKI, the brunt falls on the epithelial and endothelial cells, the fact that underlies the development of tubular epithelial and vascular compromise.This chapter further summarizes the involvement of several cell organelles in AKI: mitochondrial involvement in perturbed energy metabolism, lysosomal involvement in degradation of misfolded proteins and damaged organelles, and peroxisomal involvement in the regulation of oxidative stress and metabolism, all of which become defective. Common molecular pathways are engaged in cellular stress response and their roles in cell death or survival. The diverse families of nephrotoxic medications and the respective mechanisms they induce AKI are discussed. The mechanisms of action of some nephrotoxins are analysed, and also of the preventive therapies of ischaemic or pharmacologic pre-conditioning.An emerging concept of the systemic inflammatory response triggered by AKI, which can potentially aggravate the local injury or tend to facilitate the repair of the kidney, is presented. Rational therapeutic strategies should be based on these well-established pathophysiological hallmarks of AKI.

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42

Abcejo, Arnoley S., and Jeffrey J. Pasternak. Neurogenic Shock. Edited by Matthew D. McEvoy and Cory M. Furse. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190226459.003.0072.

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Neurogenic shock is a pathophysiologic state of systemic hypoperfusion characterized by a significant decrease in systemic vascular resistance secondary to loss of sympathetic tone. Neurogenic shock is most commonly seen in the setting of acute spinal cord injury (SCI) but can also occur following significant brain injury. Interruption of sympathetic fibers causes loss of basal vascular sympathetic tone, commonly allowing unopposed parasympathetic tone. As a result, severe hypotension and bradycardia can further exacerbate neurologic injury and organ perfusion. Understanding the physiologic and anatomic changes of neurogenic shock can help direct appropriate resuscitation efforts. Physiologic goals should focus on reversing hypotension, preventing hypoxia, and optimizing perfusion of the injured central nervous system and other critical organs.

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43

Flower, Oliver, and Matthew Mac Partlin. Pathophysiology, causes, and management of non-traumatic spinal injury. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0242.

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Non-traumatic spinal cord injury (NTSCI) is at least as common as traumatic spinal cord injury (TSCI). It affects both sexes equally and an older population than TSCI. It is a devastating condition with immense functional implications for the individuals involved. There is a wide spectrum of aetiologies with varying pathophysiology and knowledge of these is important to avoid delay in diagnosis and time-critical treatment. The most common causes described in case series in developed countries are degenerative disc disease, canal stenosis, tumours, vascular diseases and inflammatory conditions. History and examination may help direct investigations, but magnetic resonance imaging is usually required. Management of NTSCI focuses on diagnosing and treating the precipitating cause, supportive management, and preventing complications. The outcomes of non-traumatic spinal cord injury are similar to those of traumatic spinal cord injury and depend on the grade and level of injury, pre-morbid status, and concurrent co-morbidities.

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44

Tsai, Ching-Wei, Sanjeev Noel, and Hamid Rabb. Pathophysiology of Acute Kidney Injury, Repair, and Regeneration. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199653461.003.0030.

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Acute kidney injury (AKI), regardless of its aetiology, can elicit persistent or permanent kidney tissue changes that are associated with progression to end-stage renal disease and a greater risk of chronic kidney disease (CKD). In other cases, AKI may result in complete repair and restoration of normal kidney function. The pathophysiological mechanisms of renal injury and repair include vascular, tubular, and inflammatory factors. The initial injury phase is characterized by rarefaction of peritubular vessels and engagement of the immune response via Toll-like receptor binding, activation of macrophages, dendritic cells, natural killer cells, and T and B lymphocytes. During the recovery phase, cell adhesion molecules as well as cytokines and chemokines may be instrumental by directing the migration, differentiation, and proliferation of renal epithelial cells; recent data also suggest a critical role of M2 macrophage and regulatory T cell in the recovery period. Other processes contributing to renal regeneration include renal stem cells and the expression of growth hormones and trophic factors. Subtle deviations in the normal repair process can lead to maladaptive fibrotic kidney disease. Further elucidation of these mechanisms will help discover new therapeutic interventions aimed at limiting the extent of AKI and halting its progression to CKD or ESRD.

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45

Levi, Marcel, and Tom van der Poll. Coagulation and the endothelium in acute injury in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0307.

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Vascular endothelial cells play a pivotal mediatory role in many responses to systemic inflammation, including the cross-talk between coagulation and inflammation in sepsis. Endothelial cells respond to the cytokines expressed and released by activated leukocytes, but can also release cytokines themselves. Furthermore, endothelial cells are able to express adhesion molecules and growth factors that may not only promote the inflammatory response further, but also affect a myriad of downstream responses. It has recently become clear that, in addition to these mostly indirect effects of the endothelium, injured endothelial cells directly interfere with platelet-vessel wall interactions, neutrophil entrapment through formation of extracellular nets, and activation of inflammation and coagulation mediated by microparticles. The role of the glycocalyx as an important interface between the endothelium and regulation of coagulation in inflammatory states has also gained a lot of recent attention.

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46

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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47

McDougall, Robert. Management of Acutely Burned Children. 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/9780190678333.003.0021.

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The general approach for a child who has suffered burns, as for any injured child, should be assessment and management of airway, breathing, and circulation (ABC). A child status post-burn injury may require immediate intubation due to smoke inhalation and ensuing respiratory distress. The resuscitation of the child with burn injury poses a number of challenges to the anesthesiologist and requires an understanding of the pathophysiology of this type of injury. Appropriate vascular access and pain management are also of high priority in this scenario. This chapter discusses the approach to resuscitation of the child with acute burn injuries, reviews the key issues in developing a plan to secure the airway, and describes effective pain management in the setting of an acute burn.

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48

Reich, David L., Stephan A. Mayer, and Suzan Uysal, eds. Neuroprotection in Critical Care and Perioperative Medicine. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190280253.001.0001.

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Clinicians caring for patients are challenged by the task of protecting the brain and spinal cord in high-risk situations. These include following cardiac arrest, in critical care settings, and during complex procedural and surgical care. This book provides a comprehensive overview of various types of neural injury commonly encountered in critical care and perioperative contexts and the neuroprotective strategies used to optimize clinical outcomes. In addition to introductory chapters on the physiologic modulators of neural injury and pharmacologic neuroprotectants, the topics covered include: imaging assessment; tissue biomarker identification; monitoring; assessment of functional outcomes and postoperative cognitive decline; traumatic brain injury; cardiac arrest and heart-related issues such as valvular and coronary artery bypass surgery, aortic surgery and stenting, and vascular and endovascular surgery; stroke; intracerebral hemorrhage; mechanical circulatory support; sepsis and acute respiratory distress syndrome; neonatal issues; spinal cord injury and spinal surgery; and issues related to general, orthopedic, peripheral vascular, and ear, nose and throat surgeries.

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49

Narouze, Samer N. Cervical Sympathetic Block: Ultrasound. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199908004.003.0028.

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To improve the safety of the stellate ganglion block (SGB), the techniques for SGB have evolved over time from the standard blind technique to fluoroscopy and more recently to ultrasound-guided technique. Ultrasound-guided SGB may also improve the safety of the procedure by direct visualization of vascular structures and soft-tissue structures. Accordingly, the risk of vascular and soft-tissue injury may be minimized. Ultrasound guidance will allow direct monitoring of the spread of the injectate and hence may minimize complications such as recurrent laryngeal nerve (RLN) palsy and intrathecal, epidural, or intravascular spread.

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50

Alikhan, Raza. Normal haemostatic function. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0283.

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Humans have evolved an intricate system that maintains blood in a fluid state. This relies on an intact vascular endothelium modulating vascular tone and forming a barrier between blood components and reactive subendothelial components. It also involves the production of inhibitors of both blood coagulation and platelet aggregation. In addition, haemostatic systems are primed to convert blood from its fluid state to a solid state, to allow the formation of a haemostatic plug, following vessel injury, to stem the flow of blood from or within a blood vessel. This chapter reviews the physiology of haemostasis.

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Books on the topic 'Vascular injury'

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