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Thrombosis Information - Other


Should a patient with primary intracerebral haemorrhage receive antiplatelet or anticoagulant therapy?

BMJ 2005;331:439-442 (20 August), doi:10.1136/bmj.331.7514.439

Inferior Vena Cava Filters

The treatment of choice for deep venous thrombosis (DVT) and pulmonary embolism (PE) is anticoagulant therapy. Inferior vena cava (IVC) filters have been developed to prevent PE in patients with venous thromboembolism who have a contraindication to anticoagulation or in patients considered to be at very high for PE. Several recent reviews are recommended. Percutaneous IVC filters are either permanent or retrievable. The latter are also called optional filters, because they can be retrieved when no longer needed, or they can be left in place as permanent devices. The indications for IVC filter placement, the selection of a filter type, and the management after filter insertion are all very controversial issues because there is little prospectively derived data6 and only a single randomized clinical trial has been conducted in this area.

Clotting Disorders Presentation

This presentation on inherited and acquired blood clotting disorders was presented in Columbus, OH in May, 2006 at the patient education seminar presented by the National Alliance for Thrombosis and Thrombophilia. The presenter is Stephan Moll, M.D. from the University of North Carolina, Chapel Hill.

Venous Thrombosis: The Role of Genes, Environment, and Behavior

Hematology 2005 © 2005 The American Society of Hematology. Over the last decade we have witnessed an avalanche of newly identified risk factors for venous thrombosis. This has advanced our knowledge of its etiology, because more determinants have been described and because the underlying concepts have received a new and broader understanding. Venous thrombosis is a common multicausal disease occurring as the result of interacting genetic, environmental and behavioral risk factors. Some of these have been known since medieval times, such as the increased risk of thrombosis during immobilization in pregnancy and after childbirth (although retained milk of the breast-feeding mother was seen as the primary cause for the latter). Pregnancy and puerperium still cause thrombosis, as do exogenous hormones in oral contraceptives and hormonal replacement therapy. Furthermore, the immobilization in the puerperium of the old days translates directly to situations of immobilization in current times, such as prolonged travel in airplanes or excessive electronic gaming. While pedigrees with abundant thrombosis were observed in the early 1900s, the first cause of heritable thrombophilia (antithrombin deficiency) was discovered in 1965, with the subsequent identification of deficiencies of protein C and protein S in the early 1980s. These were uncommon and strong risk factors, whereas the more recently discovered genetic variants are common and weak, and cause disease only in the presence of other factors.

Blood or organ donation and thrombophilia

Last Updated: 9/13/05

The facts on post-thrombotic syndrome

Venous thrombosis is the development of a blood clot in a vein. Sometimes, thrombosis leads to serious short-term and long-term effects. A possible short-term effect is pulmonary embolism, in which the blood clot breaks into pieces, travels to the lungs and blocks the flow of blood through the lungs. Long-term effects are known as post-thrombotic syndrome. If you have had a venous thrombosis, you may be at risk of developing post-thrombotic syndrome.

Cost Implications of Using Unfractionated Heparin or Enoxaparin in Medical Patients at Risk for Venous Thromboembolic Events

322 P&T® • June 2006 • Vol. 31 No. 6. Conclusion. Enoxaparin was associated with lower total inpatient costs of care than UFH for preventing VTE in hospitalized at-risk patients.

Lower Extremity Venous Anatomy and the use of Ultrasound for Detecting and Diagnosing Thrombus By: Erika Godfrey

Quick lesson of veins in the legs as well as information on "decoding" the lingo of ultrasound diagnosis

Can causes of false-normal D-dimer test [SimpliRED] results be identified?

Thromb Res. 2003;111(3):155-8.

eMedicine - Cerebral Venous Thrombosis Article by W Alvin McElveen, MD

Thrombosis of the venous channels in the brain is an uncommon cause of cerebral infarction relative to arterial disease but is an important consideration because of its potential morbidity. Venous thrombosis may occur with headache and cranial nerve palsies. Newer imaging procedures have led to easier recognition of venous sinus thrombosis, offering the opportunity for early therapeutic measures. Venous thrombosis also may be associated with other medical complications that require therapeutic intervention. Last Updated: October 3, 2006

Post-Thrombotic Syndrome

Post-thrombotic syndrome is the name used to describe the long-term effects that can occur after you have had a venous thrombosis of the deep veins of the leg. It is caused by damage to the veins, resulting in higher than normal blood pressure. This increased pressure on the vein walls can damage the valves, which normally work to keep blood flowing properly through your veins. Poor blood flow can lead to pain, swelling and leg ulcers, which are some of the symptoms of post-thrombotic syndrome. Post-thrombotic syndrome can cause serious long-term ill health, poor quality of life, and increased costs for the patient and the healthcare system. Last modified: 19-Dec-2003

Can you recognize a patient at risk for a hypercoagulable state?

CME - Allan Platt, PA-C, MMSc, December 01, 2008

Blood Chemistry Definitions


Disseminated Intravascular Coagulation

Disseminated intravascular coagulation (DIC) is a complex systemic thrombohemorrhagic disorder involving the generation of intravascular fibrin and the consumption of procoagulants and platelets. The subcommittee on DIC of the International Society on Thrombosis and Hemostasis has suggested the following definition for DIC: "An acquired syndrome characterized by the intravascular activation of coagulation with loss of localization arising from different causes. It can originate from and cause damage to the microvasculature, which if sufficiently severe, can produce organ dysfunction".

The Epidemiology of Venous Thromboembolism in the Community

Arteriosclerosis, Thrombosis, and Vascular Biology. 2008;28:370. © 2008 American Heart Association, Inc.

TIGC Clinical Guides

This site is designed as a resource for the health care professional. Please note that these recommendations must be viewed as general guidelines based on current knowledge. Their application must be adapted to individual patients. The Thrombosis Interest Group assumes no responsibility or liability arising from any error or omission or from the use of any information contained herein. Once you click for access there will be numerous articles that will appear.

Report Suggests a Connection between Blood Type and DVT Risk

Source: Obesity, Fitness & Wellness Week, September 3, 2005

Venous Insufficiency

Article by Craig Feied, MD, FACEP, FAAEM, FACPh In venous insufficiency states, venous blood escapes from its normal antegrade path of flow and refluxes backward down the veins into an already congested leg. Venous insufficiency syndromes are caused by valvular incompetence in the high-pressure deep venous system, low-pressure superficial venous system, or both. Untreated venous insufficiency in the deep or superficial system causes a progressive syndrome involving pain, swelling, skin changes, and eventual tissue breakdown. Last Updated: September 14, 2005

Birth control options in thrombophilia

While progestin-only contraceptives do not increase the risk of thrombosis in the general population, it is not known whether they may increase the risk for thrombosis in people who (a) have had a previous clot or (b) have factor V Leiden or another thrombophilia. In the absence of data I think it is fair to conclude that one can not rule out a small increased risk of thrombosis with progestin-only contraceptives. The concern about a potential thrombophilic risk of progestin-only contraceptives stems from the fact that progestins used at higher doses for other purposes than contraception (dysfunctional uterine bleeding, amenorrhea) may be associated with an increased risk of thrombosis. This is a scientific field that is evolving and hopefully at some point in the future we will have data as to whether progestin-only contraceptives increase the risk for thrombosis in thrombosis-prone individuals or not. Progestin-only contraceptives are: Oral pills Micronor®, Ovrette®, NOR-QD®. Depo-Provera (= depot medroxy-progesterone) Mircette® IUD

Derivation of a Clinical Decision Rule to Decrease the Rate of False-positive D-dimer Assays in Emergency Department Patients Evaluated for Pulmonary Embolism

Acad Emerg Med Volume 12, Number 5_suppl_1 42, © 2005 Society for Academic Emergency Medicine Academic Emergency Medicine Volume 12, Number 5 suppl 1 42, © 2005 Society for Academic Emergency Medicine Michael S. Runyon, William B. Webb, Alan E. Jones and Jeffrey A. Kline

False-Positive D-Dimer Result in a Patient With Castleman Disease

Archives of Pathology & Laboratory Medicine, Mar 2004 by Mugler, Kimberly, Lefkowitz, Jerry B

The Assessment and Management of Venous Thromboembolism

Nursing Standard. 20, 28, 58-64. September 9, 2005

Venous Thromboembolism: Application and Effectiveness of the American College of Chest Physicians 2001 Guidelines for Prophylaxis

JAOA • Vol 106 • No 7 • July 2006 • 388-395. Conclusions: Adherence to the ACCP guidelines is suboptimal, with a substantial proportion of patients with VTE receiving inadequate prophylaxis. The additional finding that the incidence of VTE is high despite adequate prophylaxis indicates that the guidelines may need to be reevaluated.

D-dimer

Also known as: Fragment D-dimer, Fibrin degradation fragment This page was last modified on December 29, 2004.

Platelet Glycoprotein IIIa PlA Polymorphism, Fibrinogen, and Platelet Aggregability

(Circulation. 2001;104:140.) © 2001 American Heart Association, Inc. Higher fibrinogen levels were associated with increased platelet aggregability. However, the association between fibrinogen and platelet aggregability was genotype specific. This interaction may be responsible for the conflicting findings regarding PlA genotype and platelet aggregability. Further study of this gene-environment interaction may provide insight into cardiovascular disease risk.


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