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Books on the topic 'Deep vein thrombosis (DVT)'

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Published: 4 June 2021
Last updated: 1 February 2022

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1

Autar, Atmaram. Nursing assessment of clients at risk of deep vein thrombosis (DVT): Developing the Autar DVT scale. Birmingham: University of Central England in Birmingham, 1994.

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2

Autar, A. R. Advancing clinical practice in the management of Deep Vein Thrombosis (DVT): Development, application and evaluation of the Autar DVT risk assessment scale. Leicester: De Montfort University, 2002.

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3

Autar, Ricky. Deep vein thrombosis: The silent killer. Wilts: Quay Books, 1996.

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4

Griffin, Jane. Deep vein thrombosis and pulmonary embolism. London: Office of Health Economics, 1996.

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5

van Beek, Edwin J. R., Harry R. Bller, and Matthijs Oudkerk, eds. Deep Vein Thrombosis and Pulmonary Embolism. Chichester, UK: John Wiley & Sons, Ltd, 2009. http://dx.doi.org/10.1002/9780470745007.

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6

Raskin, Gregory Stephen. Bedside doppler identification of lower-extremity deep-vein thrombosis. [New Haven, Conn: s.n.], 1998.

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7

F, Tapson Victor, and Ortel Thomas L. 1957-, eds. 100 questions & answers about deep vein thrombosis and pulmonary embolism. Sudbury, Mass: Jones and Bartlett Publishers, 2008.

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8

Inc, ebrary, ed. Deep vein thrombosis and pulmonary embolism: A guide for practitioners. Cumbria [England]: M&K Update Ltd., 2009.

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9

Parker, James N., and Philip M. Parker. Deep vein thrombosis: A medical dictionary, bibliography, and annotated research guide to Internet references. San Diego, CA: ICON Health Publications, 2004.

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10

Tinkler, Kerry. Setting up, piloting, implementing and reviewing a GP direct access service for the diagnosis of lower limb deep vein thrombosis. Portsmouth: University of Portsmouth, 2004.

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11

Sheares, Karen, and Joanna Pepke-Zaba. Venous thrombosis and pulmonary embolism. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0101.

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Venous thromboembolism (VTE) is a condition in which thrombus forms in a vein, commonly in the deep veins of the leg, termed deep-vein thrombosis (DVT). The thrombus may dislodge from the site of origin and be carried into the pulmonary vasculature, causing a pulmonary embolism (PE). Deep vein thrombosis and pulmonary embolism share similar predisposing factors; however, mortality is greater in those who present with PE than in those who present with DVT. Thrombi may form in other parts of the vasculature.
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12

Tasse, Jordan C., and Bulent Arslan. Management of Acute Iliocaval Thrombosis. Edited by S. Lowell Kahn, Bulent Arslan, and Abdulrahman Masrani. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199986071.003.0035.

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Acute deep vein thrombosis (DVT) occurs in approximately 300,000 people per year in the United States. Iliocaval thrombosis is most commonly related to the progression of lower extremity DVT. Inferior vena cava (IVC) thrombosis occurs in approximately 4–15% of patients with acute DVT. Vena cava thrombosis is frequently associated with neoplastic disease. Foreign body placement such as an IVC filter or a venous catheter is a frequently reported cause of iliocaval thrombosis. External compression due to right common iliac artery mass effect (May–Thurner syndrome), tumor, lymphadenopathy, or aortic aneurysm are also commonly seen. This chapter discusses the interventional measures to manage acute iliocaval thrombosis.
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13

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

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Lower extremity deep venous thrombosis (DVT) may be complicated by pulmonary embolism, post-thrombotic syndrome, and phlegmasia cerulea dolens. Due to these complications, the American Venous Forum now recommends thrombus removal for large or symptomatic thrombus burden. The AngioJet Solent Proxy and Omni thrombectomy sets are indicated for use in iliofemoral and lower extremity veins with a diameter ≥3 mm. The device has quickly become a preferred device among the available mechanical thrombectomy options. The AngioJet system has been demonstrated as both efficacious and safe as a method of thrombectomy in lower extremity DVT. This chapter discusses two techniques to utilize the AngioJet device in iliofemoral DVT.
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14

Ahmed, Osmanuddin. Management of Chronic Iliocaval Thrombosis. Edited by S. Lowell Kahn, Bulent Arslan, and Abdulrahman Masrani. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199986071.003.0036.

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Chronic deep venous thrombosis (DVT) is defined by thrombus persisting beyond 28 days of initial onset and represents a condition that leads to long-standing venous hypertension, valvular incompetence, and ultimately chronic venous insufficiency and occlusion. As chronic thrombus organizes, it contracts and becomes adherent to the vein wall, causing scarring and consequent atresia of the lumen. The sequelae of such disease are manifested by limb edema, pain, discoloration, exercise intolerance, and ulceration—all encompassed within a clinical spectrum known as post-thrombotic syndrome. Attempts at recanalization with venoplasty and stenting of chronic inferior vena cava (IVC) and iliac occlusions are performed to restore the main venous outflow of the extremities to reverse or arrest the morbidity associated with this disease. This chapter discusses the interventional management of chronic iliocaval thrombosis.
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15

Watson, Max, Caroline Lucas, Andrew Hoy, and Jo Wells. Palliative haematological aspects. Oxford University Press, 2010. http://dx.doi.org/10.1093/med/9780199234356.003.0023.

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This chapter on palliative haematological aspects covers anaemia in chronic disorders, blood transfusion, erythropoietin, bleeding and haemorrhage, blood products, bleeding directly related to cancer, haemoptysis, haematemesis, rectal bleeding, haematuria, massive terminal haemorrhage, thromboembolism, deep vein thrombosis (DVT), pulmonary embolism (PE), chronic venous thrombosis, warfarin in patients with cancer, and developing a good relation with haematology colleagues.
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16

News, PM Medical Health. 21st Century Complete Medical Guide to Thrombophlebitis, Deep Vein Thrombosis (DVT), and Pulmonary Embolism, Authoritative Government Documents, Clinical ... Information for Patients and Physicians. Progressive Management, 2004.

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17

Loochtan, Aaron I., Jodi Dodds, and Cheryl D. Bushnell. Hemorrhagic Stroke Management in Pregnancy. Edited by Emma Ciafaloni, Cheryl Bushnell, and Loralei L. Thornburg. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190667351.003.0015.

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Intracerebral hemorrhage (ICH) during pregnancy and the puerperuim is a rare but potentially devastating complication of pregnancy. It is a condition that requires emergent medical attention and inclusion of multiple medical and or surgical specialists. Accurate diagnosis based on clinical exam and supported by neuroimaging techniques is essential. Medical management is the mainstay in most cases including post-hemorrhage blood product consideration, reversal agents if on anti-coagulation, blood pressure control, cerebral edema management, and treatment of seizures. Circumstances also arise in which surgical intervention is needed. It is important to also discuss optimal timing of delivery. Postpartum care including close blood pressure control, deep vein thrombosis prophylaxis (DVT), and risk factor modification are important. Ethical situations sometimes arise and must also be considered with respect to the mother and child.
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18

Deep Vein Thrombosis. Taylor & Francis Group, 2013.

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19

Lorenzo, F. De. Deep Vein Thrombosis. Taylor & Francis, 1997.

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20

Cheng, Gregory, ed. Deep Vein Thrombosis. InTech, 2012. http://dx.doi.org/10.5772/1171.

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21

Katritsis, Demosthenes G., Bernard J. Gersh, and A. John Camm. Deep vein thrombosis. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199685288.003.1733_update_003.

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22

Company, Anatomical Chart. Deep Vein Thrombosis Anatomical Chart. Lippincott Williams & Wilkins, 2003.

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23

Beek, Edwin J. R. van., Büller H. R, and Oudkerk Matthijs, eds. Deep vein thrombosis and pulmonary embolism. Chichester, West Sussex: J. Wiley, 2009.

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24

Deep vein thrombosis and pulmonary embolism. Chichester, West Sussex: J. Wiley, 2009.

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25

Deep Vein Thrombosis: Symptoms, Diagnosis and Treatments. Nova Science Pub Inc, 2012.

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26

Deep Vein Thrombosis (Key Management Skills in Nursing). Quay Books,a division of Mark Allen Publishing Ltd, 1996.

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27

Deep-Vein Thrombosis: Risk Factors, Treatment and Clinical Outcomes. Nova Science Pub Inc, 2014.

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28

Thomas, Stephen. Graduated external compression and prevention of deep vein thrombosis. Surgical Materials Testing Laboratory, 1992.

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29

Andrew N. Nicolaides MS FRCS FRCSE and David S. Sumner MD. Investigation of Patients with Deep Vein Thrombosis and Chronic Venous Insufficiency. Med-Orion Publishing Co Ltd, 1991.

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30

Nicolaides, Andrew N. Investigation of patients with deep vein thrombosis and chronic venous insufficiency. Med-Orion, 1991.

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31

Fan-Lun, Chris. Analysis of anti-xa levels in deep venous thrombosis (DVT) patirnts treated with dalteparin (Fragmin). 1999.

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32

MEDI-SIM. Clinical Simulations In Medical Surgical Nursing Module 4: A PATIENT WITH DEEP VEIN THROMBOSIS. Lippincott Williams & Wilkins, 1994.

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33

Publications, ICON Health. Deep Vein Thrombosis - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References. ICON Health Publications, 2004.

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34

U.S. Department of Health and Human Services. The Surgeon General's Call to Action to Prevent Deep Vein Thrombosis and Pulmonary Embolism. CreateSpace Independent Publishing Platform, 2012.

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35

The Surgeon General's call to action to prevent deep vein thrombosis and pulmonary embolism. [Rockville, MD]: U.S. Public Health Service, [Office of the Surgeon General], 2008.

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36

Bianchi, Massimiliano. Vena Cava Malformations as an Emerging Etiologic Factor for Deep Vein Thrombosis in Young Patients. INTECH Open Access Publisher, 2012.

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37

Xenoyannis, Dimitra. Development and evaluation of a patient information pamphlet for outpatient treatment of deep vein thrombosis. 1997.

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38

Gavura, S. Evaluation of a heparin nomogram in the treatment of deep vein thrombosis and pulmonary embolism. 1994.

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39

James, Andra H. 100 Q&A About Deep Vein Thrombosis and Pulmonary Embolism (100 Questions & Answers about . . .) (100 Questions & Answers). Jones and Bartlett Publishers, Inc., 2007.

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40

(Editor), G. Agnelli, and Harry R. Buller (Editor), eds. The Diagnosis of Deep Vein Thrombosis and Pulmonary Embolism (Proceedings of a Symposium, Mexico City, April 1994). S. Karger AG (Switzerland), 1995.

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41

Fritsch, Nancy. Evaluation of heparin and warfarin treatment for deep vein thrombosis and pulmonary embolism at Sunnybrook Health Science Centre. 1993.

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42

Quantrill, S. A reflective analysis of a change in practice: A standardised prophylactic regime for deep vein thrombosis and pulmonary embolism. 2003.

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43

Warwick, David. Prevention of thrombosis in orthopaedic surgery. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199550647.003.0006.

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♦ The risk–benefit of thromboprophylaxis in orthopaedic surgery remains unclear♦ Some conditions, such as major trauma, carry a much higher risk than others, such as routine knee replacement♦ Some patients appear to be genetically more predisposed than others♦ In trials of efficacy of thromboembolism, the use of deep vein thrombosis as a surrogate endpoint for death from a pulmonary embolus may not be completely reliable♦ There is a variety of mechanical and chemical methods available, each of which has real and potential advantages as well as real and potential dangers♦ Even the length of time that a patient is at risk after major surgery is unclear♦ Clinicians should adhere to guidelines where possible.
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44

Kahn, S. Lowell. Deploying a Straight Conical Filter. Edited by S. Lowell Kahn, Bulent Arslan, and Abdulrahman Masrani. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199986071.003.0053.

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Placement of inferior vena cava (IVC) filters is among the most common medical procedures, with more than 265,000 placed annually. Absolute indications for their placement include acute proximal deep venous thrombosis (DVT) and pulmonary embolism (PE) in patients who have an absolute contraindication to anticoagulation and patients with recurrent thromboembolism despite adequate anticoagulation. Although the survival benefit is unknown, it has been shown that filters decrease the incidence of PE in the short term. Unfortunately, this comes at the expense of known complications, the most important being DVT. This chapter discusses simple techniques to prevent conical filter tilting and enhance retrieval.
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45

Carton, James. Vascular pathology. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198759584.003.0003.

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This chapter covers vascular pathology, including common arterial and venous diseases including atherosclerosis and its complications, hypertension, shock, chronic lower limb ischaemia, acute lower limb ischaemia, aortic dissection, abdominal aortic aneurysm, deep vein thrombosis, and varicose veins.
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46

Cassidy, Jim, Donald Bissett, Roy A. J. Spence OBE, Miranda Payne, and Gareth Morris-Stiff. Thromboembolic and cardiac emergencies. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199689842.003.0034.

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Describes the incidence and aetiology of excessive clotting and / or bleeding diathesis in cancer. This includes descriptions of disseminated intravascular coagulation, deep vein thrombosis. Outlines investigations and immediate therapy options.Also discusses cardiac events including pericardial effusions. Describes aetiology, pathophysiology, investiagation and therapy of this medical emergency.
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47

Patel, Mikin V., and Steven Zangan. Femoral Retrieval of Conical Filters. Edited by S. Lowell Kahn, Bulent Arslan, and Abdulrahman Masrani. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199986071.003.0056.

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Inferior vena cava (IVC) filters are a safe, effective treatment option for the prevention of pulmonary embolism in patients who either have contraindication to or fail anticoagulation. However, filters pose long-term risks, such as IVC thrombosis, deep vein thrombosis, penetration of the IVC wall, filter fracture, and filter migration. IVC filters should be retrieved once the indication for placement has passed. However, cervical access frequently becomes compromised. This chapter reviews strategies for retrieving IVC filters from a femoral approach. Various techniques are discussed, including snaring the filter struts and the use of bilateral femoral sheaths to recapture the IVC filter.
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48

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

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The anti-phospholipid syndrome (APS) described almost 30 years ago, is now recognized as a major cause of deep vein thrombosis, stroke, and heart attacks in young people (<45 years of age). It is also the commonest treatable cause of recurrent miscarriages and a major cause of late fetal death. Other clinical manifestations are cardiac valvular disease, livedo reticularis, renal thrombotic microangiopathy, thrombocytopenia, haemolytic anaemia, epilepsy, and cognitive impairment. The presence of anti-phospholipid antibodies (aPL) has been closely related to the development of thrombosis and complications in pregnancy. However, not all patients with aPL will develop the clinical features. Lupus anticoagulant is generally thought to be more strongly associated with the risk of clinical manifestations of APS than anticardiolipin and anti ?2-glycoprotein I antibodies. The exact pathogenic mechanisms leading to thrombosis and/or pregnancy morbidity are poorly understood. Therapy of thrombosis is based on long-term oral anti-coagulation and patients with arterial events should be treated aggressively. Obstetric care is based on combined medical-obstetric high-risk management and treatment with aspirin and heparin.
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49

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

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The anti-phospholipid syndrome (APS) described almost 30 years ago, is now recognized as a major cause of deep vein thrombosis, stroke, and heart attacks in young people (<45 years of age). It is also the commonest treatable cause of recurrent miscarriages and a major cause of late fetal death. Other clinical manifestations are cardiac valvular disease, livedo reticularis, renal thrombotic microangiopathy, thrombocytopenia, haemolytic anaemia, epilepsy, and cognitive impairment. The presence of anti-phospholipid antibodies (aPL) has been closely related to the development of thrombosis and complications in pregnancy. However, not all patients with aPL will develop the clinical features. Lupus anticoagulant is generally thought to be more strongly associated with the risk of clinical manifestations of APS than anticardiolipin and anti ?2-glycoprotein I antibodies. The exact pathogenic mechanisms leading to thrombosis and/or pregnancy morbidity are poorly understood. Therapy of thrombosis is based on long-term oral anti-coagulation and patients with arterial events should be treated aggressively. Obstetric care is based on combined medical-obstetric high-risk management and treatment with aspirin and heparin.
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50

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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