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Deep vein thrombosis

For patient information page, click here

For economy class syndrome, click here

For main page on venous thrombosis, click here

Editor(s)-In-Chief: The APEX Trial Investigators, C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2]; Kashish Goel, M.D.; Justine Cadet; Rim Halaby, M.D. [3]

Synonyms and keywords: DVT

Overview

Overview

Editor(s)-In-Chief: The APEX Trial Investigators, C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Cafer Zorkun, M.D., Ph.D. [2] ;Kashish Goel, M.D.; Assistant Editor(s)-In-Chief: Justine Cadet

Overview

Deep vein thrombosis (also known as deep venous thrombosis or DVT and colloquially referred to as economy class syndrome) is the formation of a blood clot (“thrombus”) in a deep vein. The risk is significantly increased if the thrombus embolizes to the lungs, causing pulmonary embolism. Occasionally, veins in the arm are also affected (known as Paget-Schrötter disease). Upper extremity DVT is less common but also may lead to PE, especially in the presence of a venous catheter.[1] Thrombophlebitis is swelling (inflammation) of a vein caused by a blood clot. Venous thromboembolism (VTE) is a hypernym which includes Deep venous thrombosis (DVT) and pulmonary embolism (PE). It is a major public health problem and one of the most common cause of preventable cause of death in hospital patients. It is the third most common cardiovascular disorder after coronary artery disease and stroke. It is frequently underestimated and misdiagnosed and failure to provide adequate prophylaxis and therapy can be fatal for the patient.

Classification

Deep vein thrombosis (DVT) is classified based on the site of occlusion or clot formation. Symptom presentation and complication is largely influenced by location of the embolus.

Pathophysiology

Venous thrombosis is composed of three mechanisms, collectively described as the Virchow’s triad: 1. Alterations in blood flow (stasis): Venous stasis is a major risk factor for the development of thrombosis. It occurs in certain pathological conditions (as in heart failure) wherein it causes an increase in platelet to endothelium contact and decreases the dilution of clotting factors. This increases the risk of clot formation, and it forms microthrombi, which further grow and propagate. 2. Injury to the vascular endothelium (Endothelial dysfunction): Intrinsic or secondary to external trauma, such as catheterization, can cause intimal damage and stimulate clot formation. 3. Alterations in the constitution of blood (Hypercoagulability): Abnormal changes in coagulation can increase the propensity to develop thrombosis.

Differentiating Deep Vein Thrombosis from Other Diseases

Only 25% of the patient evaluated for deep vein thrombosis (DVT) have the disease.[2] DVT is characterized by pain and swelling of the limb, which is not specific. Numerous patients with DVT are asymptomatic.

Epidemiology and Demographics

In the United States, approximately 350,000 to 600,000 new cases of venous thromboembolism are diagnosed each year. The incidence of deep vein thrombosis is estimated to be 100 cases per 100,000 persons per year. Deep vein thrombosis accounts for two-thirds of all venous thromboembolism cases. Mortality and complications from deep vein thrombosis are high: one-third of the patients develop post-thrombotic syndrome and another 30% have recurrent DVT within 10 years. In the United States, deep vein thrombosis accounts for approximately 100,000 deaths each year.

Risk Factors

The identification and minimization of risk factors is important in the management of DVT. The duration of anticoagulation is guided by the presence of thrombophilic risk factors.

Natural History, Complications and Prognosis

Thrombus formation typically begins in the calf veins and naturally progresses to the proximal veins and ultimately, breaks free from the site formation and travels to the pulmonary artery where it is called a pulmonary embolism. In many cases, patients with a thrombus can be asymptomatic until it progresses into the proximal veins.

Diagnosis

Pretest Probability

In a patient with suspected DVT, establishing pre-test probability helps in early risk stratification and appropriate use of laboratory tests and imaging modalities. Many pretest probability scoring systems are proposed for use in primary care patients, like the Wells score, Hamilton score , and AMUSE score. [3][4] When combined with pretest probability, ultrasonography and D-dimer tests are most useful in a diagnosis for DVT.

History and Symptoms

A proper history and physical exam is very important for establishing an accurate diagnosis of DVT or VTE. One of the first steps in the management of DVT is the determination of the Wells score for DVT. Out of the 10 clinical questions in the score, 9 can be ascertained solely on the basis of history and physical exam. This underscores the importance of these variables. A high index of suspicion is also necessary to diagnose DVT.

Physical Examination

The physical examination may be completely normal in patients with DVT. A high degree of suspicion is necessary for early identification of venous thrombosis, as sometimes these patients are admitted with a different complaint and a thorough physical exam gives a clue to the diagnosis.

Laboratory Findings

The lifetime incidence of DVT ranges from 2-5% in the general population. It accounts for a large number of ER visits and puts the patient at-risk for a life-threatening pulmonary embolism. The use of D-dimer after assessment of pre-test probability has been widely validated now and has led to a significant reduction in unnecessary procedures in the ER and hospital settings. This chapter will review the role of D-dimer in diagnosis of DVT. For a detailed discussion on D-dimer, please visit D-dimer.

Ultrasound

Venous ultrasound is the confirmatory test for diagnosis of DVT. The most common form is compression ultrasonography, which assesses the compressibility of femoral and popliteal veins. Diagnosis of DVT is established if the vein can not be collapsed under gentle ultrasound probe pressure. In most cases, it is performed in the proximal veins, as the risk of pulmonary embolism is much higher with that. Whole-leg ultrasound examines the deep veins of the proximal leg and calf, and it is used in cases where distal DVT is suspected. Iliac vein ultrasound may be performed, if thrombosis is suspected (e.g.: Pregnant women with swelling of the whole leg).

Venography

Venography is the “gold standard” to diagnose venous thrombosis, however it is not the preferred test in clinical settings. It includes injection of contrast into the dorsal foot vein and checking for a intraluminal filling defect that is present in more than one view.

CT

Venous thrombosis in the proximal deep veins is responsible for more than 90% of the pulmonary embolisms. Some of the investigators have suggested combined use of CT PE protocol and CT scan venography in cases of suspected DVT and PE.[5]

MRI

MRI can also be used for the diagnosis of venous thrombosis, however it is usually not applied as a first test because of cost and inaccessibility.

Other Imaging Findings

A number of invasive and non-invasive approaches are possible.[6]

Specific Situations

The approach to diagnosis of DVT may be modified in certain situations, where the suspicion is high or there is a recurrent episode. This chapter will discuss these modifications that have been recommended to the American College of Chest Physicians.[7]

Treatment

Medical Therapy

An approach to the treatment of DVT has been described here. The primary purpose of treatment is to prevent the further clot extension, acute pulmonary embolism, recurrence of thrombosis, prevention of late complications such as post-thrombotic syndrome and chronic thromboembolic pulmonary hypertension.

Primary Prevention

Primary prevention includes the strategies that help to avoid the development of disease. Awareness of Deep venous thrombosis is the best way to prevent this condition.

Secondary Prevention

The U.S. Preventive Services Task Forces describes secondary prevention measures as those that identify and treat asymptomatic persons who have already developed risk factors or preclinical disease but in whom the condition is not clinically apparent. Clinical practice guidelines by the American College of Chest Physicians (ACCP) provide recommendations on DVT prophylaxis in hospitalized patients.[8]

Landmark Trials

Landmark trials have compared different formulations and routes of antithrombin administration to treat and prevent deep vein thrombosis.

References

  1. ↑ Ramzi DW, Leeper KV (2004). “DVT and pulmonary embolism: Part I. Diagnosis”. Am Fam Physician. 69 (12): 2829–36. PMID 15222648.
  2. ↑ Huisman MV, Büller HR, ten Cate JW, Vreeken J (1986). “Serial impedance plethysmography for suspected deep venous thrombosis in outpatients. The Amsterdam General Practitioner Study”. N Engl J Med. 314 (13): 823–8. doi:10.1056/NEJM198603273141305. PMID 3951515.
  3. ↑ Subramaniam RM, Chou T, Heath R, Allen R (2006). “Importance of pretest probability score and D-dimer assay before sonography for lower limb deep venous thrombosis”. AJR Am J Roentgenol. 186 (1): 206–12. doi:10.2214/AJR.04.1398. PMID 16357403. Retrieved 2011-12-22. Unknown parameter |month= ignored (help)
  4. ↑ van der Velde EF, Toll DB, Ten Cate-Hoek AJ, Oudega R, Stoffers HE, Bossuyt PM, Büller HR, Prins MH, Hoes AW, Moons KG, van Weert HC (2011). “Comparing the diagnostic performance of 2 clinical decision rules to rule out deep vein thrombosis in primary care patients”. Ann Fam Med. 9 (1): 31–6. doi:10.1370/afm.1198. PMC 3022042. PMID 21242558. Retrieved 2011-12-22.
  5. ↑ Kanne JP, Lalani TA (2004). “Role of computed tomography and magnetic resonance imaging for deep venous thrombosis and pulmonary embolism”. Circulation. 109 (12 Suppl 1): I15–21. doi:10.1161/01.CIR.0000122871.86662.72. PMID 15051664.
  6. ↑ Snow V, Qaseem A, Barry P, Hornbake ER, Rodnick JE, Tobolic T; et al. (2007). “Management of venous thromboembolism: a clinical practice guideline from the American College of Physicians and the American Academy of Family Physicians”. Ann Intern Med. 146 (3): 204–10. PMID 17261857.
  7. ↑ Bates SM, Jaeschke R, Stevens SM; et al. (2012). “Diagnosis of DVT: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines”. Chest. 141 (2 Suppl): e351S–418S. doi:10.1378/chest.11-2299. PMID 22315267. Unknown parameter |month= ignored (help)
  8. ↑ Geerts WH, Pineo GF, Heit JA, Bergqvist D, Lassen MR, Colwell CW, Ray JG. Prevention of venous thromboembolism: the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest. 2004 Sep;126 (3 Suppl):338S-400S. http://www.chestjournal.org/cgi/content/full/126/3_suppl/338S PMID 15383478

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Classification

Classification

Editor(s)-In-Chief: The APEX Trial Investigators, C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]; Kashish Goel, M.D.; Rim Halaby, M.D. [3] ;Assistant Editor(s)-In-Chief: Justine Cadet

Overview

Deep vein thrombosis (DVT) is classified based on the site of occlusion or clot formation into lower extremity DVT and upper extremity DVT. Lower extremity DVT can further be classified into proximal and distal. Symptoms presentation of DVT and complications are largely influenced by the location of the thrombus.

Classification

Classification Based on Site of Thrombus Formation

 
 
 
Deep vein thrombosis (DVT)
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Lower extremity DVT
 
Upper extremity DVT
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Proximal
(popliteal, femoral, and/or iliac veins)
 
Isolated distal
(calf veins)
 
 

In studies including symptomatic inpatients, 80% of DVTs are proximal and isolated distal DVT accounts for only 20% of all DVTs.[1][2][3]

Proximal Vein Thrombosis

Proximal vein thrombosis involves the proximal veins, including the popliteal, femoral, or iliac vein. Proximal vein thrombosis is responsible for the majority of acute pulmonary emboli and is associated with higher mortality.[4] Clinically, proximal vein thrombosis is considered severe, and it is more commonly associated with serious chronic diseases than distal DVT, such as:[5]

Shown below is the distribution of involved veins in proximal DVT:[3]

Distal Vein Thrombosis

Distal or calf deep vein thrombosis involves the infrapopliteal veins [ie, posterior tibial veins, peroneal veins, anterior tibial veins and muscular calf veins (soleal or gemellar veins)]. It is often associated with transient risk factors, such as:[4]

  • Recent surgery
  • Immobilization
  • Travel

It may also be associated with permanent risk factors such as:

  • Hypercoaguable state (genetic predisposition)
  • May Thurner Syndrome

Upper Extremity DVT

  • Risk of embolization in upper extremity DVT is less than that with lower extremity DVT.[9]

Classification Based on the Acuity of the Clinical Presentation

  • Subacute and acute DVT can be differentiated not only through the timing of the clinical presentation, bust also through ultrasound findings.[10]
  • Subacute thrombosis refers to thrombosis formation involving a narrowing of the vein involved and a hyperechogenic clot; flow may be partially obstructed by this narrowing.
  • Acute thrombosis can refer to:
  • A vein with a thrombus that is normal or, even, wider than usual with the contralateral side of the vein being unaffected.
  • A clot that, during ultrasound echos, is not dense.
  • A clot that may totally or partially obstruct blood flow.
  • In the evaluation of the upper extremity, the subclavian and brachiocephalic veins inability to be compressed may pose challenges for determining subacute versus acute status.

References

  1. ↑ Anand SS, Wells PS, Hunt D, Brill-Edwards P, Cook D, Ginsberg JS (1998). “Does this patient have deep vein thrombosis?”. JAMA. 279 (14): 1094–9. PMID 9546569. Unknown parameter |month= ignored (help)
  2. ↑ Wells PS, Hirsh J, Anderson DR; et al. (1995). “Accuracy of clinical assessment of deep-vein thrombosis”. Lancet. 345 (8961): 1326–30. PMID 7752753. Unknown parameter |month= ignored (help)
  3. ↑ 3.0 3.1 Cogo A, Lensing AW, Prandoni P, Hirsh J (1993). “Distribution of thrombosis in patients with symptomatic deep vein thrombosis. Implications for simplifying the diagnostic process with compression ultrasound”. Arch. Intern. Med. 153 (24): 2777–80. PMID 8257253. Unknown parameter |month= ignored (help)
  4. ↑ 4.0 4.1 Galanaud JP, Sevestre-Pietri MA, Bosson JL, Laroche JP, Righini M, Brisot D, Boge G, van Kien AK, Gattolliat O, Bettarel-Binon C, Gris JC, Genty C, Quere I (2009). “Comparative study on risk factors and early outcome of symptomatic distal versus proximal deep vein thrombosis: results from the OPTIMEV study”. Thromb. Haemost. 102 (3): 493–500. doi:10.1160/TH09-01-0053. PMID 19718469. Retrieved 2011-12-14. Unknown parameter |month= ignored (help)
  5. ↑ Alberts JL, Hass CJ, Vitek JL, Okun MS (2008). “Are two leads always better than one: an emerging case for unilateral subthalamic deep brain stimulation in Parkinson’s disease”. Exp Neurol. 214 (1): 1–5. doi:10.1016/j.expneurol.2008.07.019. PMC 2888769. PMID 18718469.
  6. ↑ 6.0 6.1 Joffe HV, Kucher N, Tapson VF, Goldhaber SZ (2004). “Upper-extremity deep vein thrombosis: a prospective registry of 592 patients”. Circulation. 110 (12): 1605–11. doi:10.1161/01.CIR.0000142289.94369.D7. PMID 15353493. Retrieved 2012-10-07. Unknown parameter |month= ignored (help)
  7. ↑ Isma N, Svensson PJ, Gottsäter A, Lindblad B (2010). “Upper extremity deep venous thrombosis in the population-based Malmö thrombophilia study (MATS). Epidemiology, risk factors, recurrence risk, and mortality”. Thromb Res. 125 (6): e335–8. doi:10.1016/j.thromres.2010.03.005. PMID 20406709.
  8. ↑ Muñoz FJ, Mismetti P, Poggio R, Valle R, Barrón M, Guil M; et al. (2008). “Clinical outcome of patients with upper-extremity deep vein thrombosis: results from the RIETE Registry”. Chest. 133 (1): 143–8. doi:10.1378/chest.07-1432. PMID 17925416.
  9. ↑ 9.0 9.1 Kucher N (2011). “Clinical practice. Deep-vein thrombosis of the upper extremities”. N Engl J Med. 364 (9): 861–9. doi:10.1056/NEJMcp1008740. PMID 21366477.
  10. ↑ Cassou-Birckholz MF, Engelhorn CA, Salles-Cunha SX, Engelhorn AL, Zanoni CC, Gosalan CJ; et al. (2011). “Assessment of deep venous thrombosis by grayscale median analysis of ultrasound images”. Ultrasound Q. 27 (1): 55–61. doi:10.1097/RUQ.0b013e31820e157d. PMID 21343802.

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Pathophysiology

Pathophysiology

Editor(s)-In-Chief: The APEX Trial Investigators, C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Cafer Zorkun, M.D., Ph.D. [2] ; Kashish Goel, M.D.; Assistant Editor(s)-In-Chief: Justine Cadet

Overview

Deep vein thrombosis (DVT) results from the formation of a blood clot in the deep veins. Three mechanisms predispose to DVT, they are collectively described as the Virchow’s triad. 1. Alterations in blood flow (stasis): Venous stasis is a major risk factor for the development of thrombosis. It occurs in certain pathological conditions (as in heart failure) wherein it causes an increase in platelet to endothelium contact and decreases the dilution of clotting factors. This increases the risk of clot formation, and it forms microthrombi, which further grow and propagate. 2. Injury to the vascular endothelium (Endothelial dysfunction): Intrinsic or secondary to external trauma, such as catheterization, can cause intimal damage and stimulate clot formation. 3. Alterations in the constitution of blood (Hypercoagulability): Abnormal changes in coagulation can increase the propensity to develop thrombosis.

Pathophysiology

Virchow’s Triad

Figure 1. Virchow's triad conceptually encompasses three broad categories of factors that are thought to contribute to venous thrombosis.

Shown below is a table depicting the elements of Virchow’s triad and their modern counterparts.

Virchow’s[3] Modern Notes
Phenomena of interrupted blood-flow “Stasis” or “venous stasis“[4] The first category, alterations in normal blood flow, refers to several situations. These include turbulence, stasis, mitral stenosis, and varicose veins. The equivalence of Virchow’s version and the modern version has been disputed.[5]
Phenomena associated with irritation of the vessel and its vicinity “Endothelial injury” or “vessel wall injury” The second category, injuries and/or trauma to endothelium includes damage to the veins arising from shear stress or hypertension.
Phenomena of blood–coagulation “Hypercoagulability” The last category, alterations in the constitution of blood,[6] has numerous possible risk factors such as hyperviscosity, deficiency of antithrombin III, nephrotic syndrome, changes after severe trauma or burn, disseminated cancer, late pregnancy and delivery, race, age, whether the patient is a smoker, and obesity. All of these risk factors lead to hypercoagulability.

Thrombus Formation

Shown below is an image depicting a thrombus formed in the deep vein of the leg.

Thrombus in the deep vein of the leg
Source: Wikipedia [7]


Venous Insufficiency

Special Conditions

Video: The Process of Thrombosis

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Pathophysiology in Upper Extremity DVT

  • While approximately 80% of upper extremity DVT are secondary, only 20% of the cases are primary.[8]

References

  1. ↑ April Wang Armstrong; David E. Golan; Armen H. Tashjian; Ehrin Armstrong (2008). Principles of pharmacology: the pathophysiologic basis of drug therapy. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. p. 396. ISBN 0-7817-8355-0.
  2. ↑ Bagot CN, Arya R (2008). “Virchow and his triad: a question of attribution”. Br. J. Haematol. 143 (2): 180–90. doi:10.1111/j.1365-2141.2008.07323.x. PMID 18783400. Unknown parameter |month= ignored (help)
  3. ↑ Agutter, Paul S. (2008). The Aetiology of Deep Venous Thrombosis: A Critical, Historical and Epistemological Survey. Berlin: Springer. p. 84. ISBN 1-4020-6649-X.
  4. ↑ Lowe GD (2003). “Virchow’s triad revisited: abnormal flow”. Pathophysiol. Haemost. Thromb. 33 (5–6): 455–7. doi:10.1159/000083845. PMID 15692260.
  5. ↑ “Further reflections on Virchow’s triad. – Free Online Library”. Retrieved 2009-02-10.
  6. ↑ Chung I, Lip GY (2003). “Virchow’s triad revisited: blood constituents”. Pathophysiol. Haemost. Thromb. 33 (5–6): 449–54. doi:10.1159/000083844. PMID 15692259.
  7. ↑ Blausen.com staff (2014). “Medical gallery of Blausen Medical 2014”. WikiJournal of Medicine 1 (2). DOI:10.15347/wjm/2014.010. ISSN 2002-4436. – Obra do próprio
  8. ↑ 8.0 8.1 8.2 Kucher N (2011). “Clinical practice. Deep-vein thrombosis of the upper extremities”. N Engl J Med. 364 (9): 861–9. doi:10.1056/NEJMcp1008740. PMID 21366477.

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Causes

Causes

Editor(s)-In-Chief: The APEX Trial Investigators, C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2]; Ogheneochuko Ajari, MB.BS, MS [3]; Kashish Goel, M.D.; Assistant Editor(s)-In-Chief: Justine Cadet

Overview

The cause of deep vein thrombosis (DVT) is the formation of a blood clot in the deep veins. Several factors predispose to DVT; however they are referred to as either risk factors or triggers. The word risk factors refers to those epidemiologic and genetic variables that expose someone to a higher risk of developing venous thrombosis. The word triggers refer to those factors in the patients immediate history or environment that may have led to the occurrence of the venous thrombosis. Risk factors and triggers of DVT are discussed elsewhere.

Causes

Life Threatening Causes

Deep venous thrombosis can be a life-threatening condition if thromboembolism and subsequent pulmonary embolism occur, and it must be treated as such irrespective of the underlying cause.

Common Causes

Causes by Organ System

Cardiovascular Antithrombin III deficiency, blood clot, congestive heart failure, May-Thurner syndrome, multifocal fibrosclerosis, Paget-Schroetter disease, thrombosis
Chemical/Poisoning No underlying causes
Dental No underlying causes
Dermatologic No underlying causes
Drug Side Effect Erythropoietin, Estradiol valerate and estradiol valerate/dienogest, Ethinylestradiol, Etonogestrel, fibrinogen,heparin-induced thrombocytopenia, hormone replacement therapy, Interferon gamma, lenalidomide, Medroxyprogesterone, Methoxy polyethylene glycol-epoetin beta, Methyltestosterone, oral contraceptives, Ospemifene, Piperacillin, Polidocanol, Pramipexole, Progesterone, raloxifene, Romidepsin, tamoxifen, thalidomide, Trametinib, tranexamic acid
Ear Nose Throat No underlying causes
Endocrine Functioning pancreatic endocrine tumor, glucagonoma syndrome, multifocal fibrosclerosis
Environmental No underlying causes
Gastroenterologic Inflammatory bowel disease
Genetic Paroxysmal nocturnal hemoglobinuria, protein C deficiency, protein S deficiency, prothrombin gene mutation G20210A
Hematologic Antiphospholipid syndrome, antithrombin III deficiency, blood clot, clotting disorders, essential thrombocythemia, factor V Leiden mutation, familial dysfibrinogenemia, hemorrhagic thrombocythemia, heparin-induced thrombocytopenia, myeloproliferative disorders, paroxysmal nocturnal hemoglobinuria, polycythemia vera, protein C deficiency, protein S deficiency
Iatrogenic Surgery (especially orthopedic or female pelvic surgery)
Infectious Disease Tuberculosis
Musculoskeletal/Orthopedic Fractures (especially of pelvis or leg), varicose veins
Neurologic Antiphospholipid syndrome, paraplegia, spinal cord injury, stroke
Nutritional/Metabolic Hyperhomocysteinemia
Obstetric/Gynecologic Antiphospholipid syndrome, hormone replacement therapy, oral contraceptives, pregnancy
Oncologic Cancer, functioning pancreatic endocrine tumor, glucagonoma syndrome, malignancy, polycythemia vera
Ophthalmologic No underlying causes
Overdose/Toxicity No underlying causes
Psychiatric No underlying causes
Pulmonary No underlying causes
Renal/Electrolyte Nephrotic syndrome
Rheumatology/Immunology/Allergy Antiphospholipid syndrome, multifocal fibrosclerosis, paraproteinemia, systemic lupus erythematosus
Sexual No underlying causes
Trauma Injury, spinal cord injury, trauma
Urologic No underlying causes
Miscellaneous Immobility, presence of a central venous catheter

Causes in Alphabetical Order

References

  1. ↑ Trabert J, Steiner T (2014). “[Deep vein thrombosis and lung embolisms in patients with stroke : Prevention and therapy.]”. Nervenarzt. doi:10.1007/s00115-014-4031-9. PMID 25186081.
  2. ↑ Singh NK, Agrawal A, Singh MN, Kumar V, Godhra M, Gupta A; et al. (2013). “Prevalence and pattern of antiphospholipid antibody syndrome in a hospital based longitudinal study of 193 patients of systemic lupus erythematosus”. J Assoc Physicians India. 61 (9): 623–6. PMID 24772699.
  3. ↑ Larsen AC, Dabrowski T, Frøkjær JB, Fisker RV, Iyer VV, Møller BK; et al. (2014). “Prevalence of venous thromboembolism at diagnosis of upper gastrointestinal cancer”. Br J Surg. 101 (3): 246–53. doi:10.1002/bjs.9353. PMID 24446107.
  4. ↑ 4.0 4.1 de Campos Guerra JC, Mourão MA, França CN, da Rosa CD, Burattini MN (2014). “Impact of coagulation in the development of thromboembolic events in patients with spinal cord injury”. Spinal Cord. 52 (4): 327–32. doi:10.1038/sc.2013.170. PMID 24513719.
  5. ↑ 5.0 5.1 Karmacharya P, Aryal MR, Donato A (2013). “Mesenteric vein thrombosis in a patient heterozygous for factor V Leiden and G20210A prothrombin genotypes”. World J Gastroenterol. 19 (43): 7813–5. doi:10.3748/wjg.v19.i43.7813. PMC 3837283. PMID 24282370.
  6. ↑ Lovecchio F (2014). “Heparin-induced thrombocytopenia”. Clin Toxicol (Phila). 52 (6): 579–83. doi:10.3109/15563650.2014.917181. PMID 24844576.
  7. ↑ 7.0 7.1 7.2 Ren W, Li Z, Fu Z, Fu Q (2014). “Analysis of risk factors for recurrence of deep venous thrombosis in lower extremities”. Med Sci Monit. 20: 199–204. doi:10.12659/MSM.889819. PMC 3930664. PMID 24500085.
  8. ↑ Wax JR, Pinette MG, Rausch D, Cartin A (2014). “May-Thurner syndrome complicating pregnancy: a report of four cases”. J Reprod Med. 59 (5–6): 333–6. PMID 24937979.
  9. ↑ Klitfod L, Broholm R, Baekgaard N (2013). “Deep venous thrombosis of the upper extremity. A review”. Int Angiol. 32 (5): 447–52. PMID 23903301.
  10. ↑ Schiffer CA, Mangu PB, Wade JC, Camp-Sorrell D, Cope DG, El-Rayes BF; et al. (2013). “Central venous catheter care for the patient with cancer: American Society of Clinical Oncology clinical practice guideline”. J Clin Oncol. 31 (10): 1357–70. doi:10.1200/JCO.2012.45.5733. PMID 23460705.
  11. ↑ Halim TA, Chhabra HS, Arora M, Kumar S (2014). “Pharmacological prophylaxis for deep vein thrombosis in acute spinal cord injury: an Indian perspective”. Spinal Cord. 52 (7): 547–50. doi:10.1038/sc.2014.71. PMID 24819510.
  12. ↑ “[Venous thromboembolic complications in patients with intracranial hemorrhage and tumors of the central nervous system]”. Khirurgiia (Mosk) (3): 49–52. 2014. PMID 24781071.
  13. ↑ Do JG, Kim du H, Sung DH (2013). “Incidence of deep vein thrombosis after spinal cord injury in Korean patients at acute rehabilitation unit”. J Korean Med Sci. 28 (9): 1382–7. doi:10.3346/jkms.2013.28.9.1382. PMC 3763116. PMID 24015047.
  14. ↑ Amin AN, Lin J, Thompson S, Wiederkehr D (2013). “Rate of deep-vein thrombosis and pulmonary embolism during the care continuum in patients with acute ischemic stroke in the United States”. BMC Neurol. 13: 17. doi:10.1186/1471-2377-13-17. PMC 3571887. PMID 23391151.
  15. ↑ Lee YK, Choi YH, Ha YC, Lim JY, Koo KH (2013). “Does venous thromboembolism affect rehabilitation after hip fracture surgery?”. Yonsei Med J. 54 (4): 1015–9. doi:10.3349/ymj.2013.54.4.1015. PMC 3663236. PMID 23709439.
  16. ↑ 16.0 16.1 Louis SG, Sato M, Geraci T, Anderson R, Cho SD, Van PY; et al. (2014). “Correlation of missed doses of enoxaparin with increased incidence of deep vein thrombosis in trauma and general surgery patients”. JAMA Surg. 149 (4): 365–70. doi:10.1001/jamasurg.2013.3963. PMID 24577627.
  17. ↑ Chung WS, Lin CL, Chang SN, Lu CC, Kao CH (2014). “Systemic lupus erythematosus increases the risks of deep vein thrombosis and pulmonary embolism: a nationwide cohort study”. J Thromb Haemost. 12 (4): 452–8. doi:10.1111/jth.12518. PMID 24472157.
  18. ↑ Pronk SM, van Ommen CH, Prince FH, Weijer O, van Rossum MA (2014). “[Venous thrombosis as a first sign of SLE]”. Ned Tijdschr Geneeskd. 158: A7179. PMID 24988153.
  19. ↑ “Tranexamic acid and thrombosis”. Prescrire Int. 22 (140): 182–3. 2013. PMID 23951593.
  20. ↑ Kechaou I, Cherif E, Ben Hassine L, Khalfallah N (2014). “Deep vein thrombosis and tuberculosis: a causative link?”. BMJ Case Rep. 2014. doi:10.1136/bcr-2013-200807. PMID 24859543.

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Differentiating Deep Vein Thrombosis from other Diseases

Differentiating Deep Vein Thrombosis from other Diseases

Editor(s)-In-Chief: The APEX Trial Investigators, C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Cafer Zorkun, M.D., Ph.D. [2] Kashish Goel, M.D.; Assistant Editor(s)-In-Chief: Justine Cadet

Overview

Deep vein thrombosis DVT is characterized by pain and swelling of the limb, which are not specific symptoms. There are other conditions that can mimic DVT such as muscle strain or muscle tear, immobilization that led to leg swelling, lymphedema, lymphangitis, chronic venous insufficiency, or cellulitis.

Differential Diagnosis

Deep vein thrombosis must be differentiated from other causes of lower limb edema like chronic venous insufficiency, lymphatic filariasis, lipedema, myxedema, cellulitis and causes of generalized edema.

Diseases Symptoms Signs Gold standard Investigation to diagnose
History Onset Pain Fever Laterality Scrotal swelling Symptoms of primary disease
Acute deep venous thrombosis Acute + – Unilateral – May be associated with primary disease mandates recumbency for long duration
Lymphatic filariasis
  • History of living in endemic area or travelling to it
 Chronic + + Bilateral + –

Preparing blood smears

  • Thick smears
  1. Thick smears consist of a thick layer of dehemoglobinized (lysed) red blood cells (RBCs).
  2. Thick smears allow a more efficient detection of parasites (increased sensitivity).
  • Thin smears consist of blood spread in a layer such that the thickness decrease.

By the ultrasound, the following findings can be observed:

  • Dilated lymphatic channels
  • Living worms tend to be in motion which called “filarial dance” sign.
Chronic venous insufficiency Chronic + – Bilateral +

(If congenial)

–
  • Typical varicose veins
  • Skin change distribution correlate with varicose veins sites in the medial side of ankle and leg
  • Reduction of swelling with limb elevation.
Lipedema Chronic + – Bilateral – –
  • Tender with palpation
  • Negative Semmer sign to differentiate from lymphedema.[3]
  • Pinching the skin on the upper surface of the toes. If it is possible to grasp a thin fold of tissue then it is negative result.
  • In a positive result, it is only possible to grasp a lump of tissue.
  • MRI offers strong qualitative and quantitative parameters in the diagnosis of lipedema [4]
Myxedema Chronic + – Bilateral – +

(hypothyroidism )

(Cellulitis–erysipelas-skin abscess) Acute + + Unilateral – –
  • Usually it doesn’t need any laboratory tests to diagnose.[6]
  • Blood cultures are warranted for patients in the following circumstances:[7]
  1. Systemic toxicity
  2. Extensive skin or soft tissue involvement
  3. Underlying comorbidities
  4. persistent cellulitis
Other causes of generalized edema
  • History of chronic general condition (cardiac-liver-renal)
 Chronic – – Bilateral – +
  • According to the primary cause ( Echo- LFTs– RFT)

Shown below is a list of conditions that can mimic DVT.

References

  1. ↑ Goodacre S, Sutton AJ, Sampson FC (2005). “Meta-analysis: The value of clinical assessment in the diagnosis of deep venous thrombosis”. Ann Intern Med. 143 (2): 129–39. PMID 16027455. Review in: ACP J Club. 2006 Mar-Apr;144(2):46-7 Review in: Evid Based Med. 2006 Apr;11(2):56
  2. ↑ Child AH, Gordon KD, Sharpe P, Brice G, Ostergaard P, Jeffery S; et al. (2010). “Lipedema: an inherited condition”. Am J Med Genet A. 152A (4): 970–6. doi:10.1002/ajmg.a.33313. PMID 20358611.
  3. ↑ Trayes KP, Studdiford JS, Pickle S, Tully AS (2013). “Edema: diagnosis and management”. Am Fam Physician. 88 (2): 102–10. PMID 23939641.
  4. ↑ Dimakakos PB, Stefanopoulos T, Antoniades P, Antoniou A, Gouliamos A, Rizos D (1997). “MRI and ultrasonographic findings in the investigation of lymphedema and lipedema”. Int Surg. 82 (4): 411–6. PMID 9412843.
  5. ↑ Stevens DL, Bisno AL, Chambers HF, Dellinger EP, Goldstein EJ, Gorbach SL; et al. (2014). “Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the infectious diseases society of America”. Clin Infect Dis. 59 (2): 147–59. doi:10.1093/cid/ciu296. PMID 24947530.
  6. ↑ Raff AB, Kroshinsky D (2016). “Cellulitis: A Review”. JAMA. 316 (3): 325–37. doi:10.1001/jama.2016.8825. PMID 27434444.
  7. ↑ Woo PC, Lum PN, Wong SS, Cheng VC, Yuen KY (2000). “Cellulitis complicating lymphoedema”. Eur J Clin Microbiol Infect Dis. 19 (4): 294–7. PMID 10834819.
  8. ↑ Leppard BJ, Seal DV, Colman G, Hallas G (1985). “The value of bacteriology and serology in the diagnosis of cellulitis and erysipelas”. Br J Dermatol. 112 (5): 559–67. PMID 4005155.
Epidemiology and Demographics

Epidemiology and Demographics

Editor(s)-In-Chief: The APEX Trial Investigators, C. Michael Gibson, M.S., M.D. [2]; Associate Editor(s)-In-Chief: Cafer Zorkun, M.D., Ph.D. [3]; Kashish Goel, M.D.; Justine Cadet; Rim Halaby, M.D. [4]

Overview

The precise number of people affected by venous thromboembolism (VTE), that is either deep vein thrombosis (DVT), pulmonary embolism (PE), or both, is unknown, but estimates range from 300,000 to 600,000 (1 to 2 per 1,000, and in those over 80 years of age, as high as 1 in 100) each year in the United States. Estimates suggest that 60,000-100,000 Americans die of VTE, 10 to 30% of which will die within one month of diagnosis. Among people who have had a DVT, one-half will have long-term complications (post-thrombotic syndrome) such as swelling, pain, discoloration, and scaling in the affected limb. One-third (about 33%) of people with VTE will have a recurrence within 10 years. Approximately 5 to 8% of the U.S. population has one of several genetic risk factors, also known as inherited thrombophilias in which a genetic defect can be identified that increases the risk for thrombosis.[1][2]

Epidemiology and Demographics

Incidence

The precise number of people affected by venous thromboembolism (VTE), that is either deep vein thrombosis (DVT), pulmonary embolism (PE), or both, is unknown, but estimates range from 300,000 to 600,000 (1 to 2 per 1,000, and in those over 80 years of age, as high as 1 in 100) each year in the United States.[1][2]

Age

The incidence of VTE increases with age, ranging from less than 5 cases per 100,000 people in childhood to 500 cases per 100,000 people in the elderly.[3] Subjects who are more than 65 years of age are at three times higher risk for VTE compared to those who are 45-54 years old.[4]

Gender

Studies about differences in the incidence of VTE by gender have mixed results. While some reported a higher incidence of DVT among young females,[5] others reported it among either older females,[6] or in men.[4][7] In addition, the risk for DVT was reported to consistently increase with age across both genders.[4]

Race

  • There is a significant difference in the incidence of DVT as it relates to race. African Americans characteristically have the highest incidence of DVT while Caucasians rank as the second highest incidence of DVT.[3]
  • When compared to African Americans and Caucasians, the incidence of DVT is noted to be two to four times lower in Hispanics and Asian-Pacific Islanders.[3]
  • Lower thrombosis incidences in non-Caucasians may be related to a lower prevalence of disorders like Factor V Leiden or Prothrombin 20210A mutation.[8][9]
  • More than 25,000 people die in England from venous thromboembolism developed in hospital. This is more than the total number of deaths attributable to breast cancer, AIDS, and road traffic accidents, when combined together.

Hospitalization for VTE

  • During 2007–2009, an estimated annual average of 547,596 hospitalizations had a diagnosis of VTE for adults aged ≥18 years. Estimates for DVT and PE diagnoses were not mutually exclusive. An estimated annual average of 348,558 adult hospitalizations had a diagnosis of DVT, and 277,549 adult hospitalizations had a diagnosis of PE. An estimated annual average of 78,511 adult hospitalizations (14% of overall VTE hospitalizations) had diagnoses of both DVT and PE.[10]
  • The estimated average annual number of hospitalizations with VTE was successively greater among older age groups: 54,034 for persons aged 18–39 years; 143,354 for persons aged 40–59 years; and 350,208 for persons aged ≥60 years. The estimated average annual number of hospitalizations with VTE was comparable for men (250,973) and women (296,623).[10] Shown below is an image depicting the estimated average annual number of hospitalization with a diagnosis of DVT, PE, or VTE by age and sex (image courtesy of CDC.gov[10]).

  • The average annual rates of hospitalizations with a discharge diagnosis of DVT, PE, or VTE among adults were 152, 121, and 239 per 100,000 population, respectively. For VTE, the average annual rates were 60 per 100,000 population aged 18–39 years, 143 for persons aged 40–49 years, 200 for persons aged 50–59 years, 391 for persons aged 60–69 years, 727 for persons aged 70–79 years, and 1,134 for persons aged ≥80 years. The rates of hospitalization were similar for men and women, and the point estimates increased for both sexes by age.[10]
  • On average, 28,726 hospitalized adults with a VTE diagnosis died each year. Of these patients, an average of 13,164 had a DVT diagnosis and 19,297 had a PE diagnosis; 3,735 had both DVT and PE diagnoses.[10]

Recurrence of VTE

  • One-third (about 33%) of people with VTE will have a recurrence within 10 years.[11][2]
  • The risk of recurrence of VTE in patients diagnosed with first-time VTE is estimated to be around 7-8 percent per year during an average follow up period of 2.2 years of subsequent observation of 265 patients.[4]
  • Among patients with a first episode of VTE, the risk of recurrence of VTE is particularly elevated in the first 6 to 12 months following the first episode of VTE. The risk of recurrent VTE remains up to 10 years, with a estimated cumulative incidence of first overall VTE recurrence of 30 %. Predictors for recurrence of VTE include malignancy, neurological diseases, and paresis.[12]
  • In recent years, the increase in thrombosis incidence may be related to improved diagnostic modalities and increased awareness by clinicians.[3]

Complications of VTE

  • Estimates suggest that 60,000-100,000 Americans die of VTE, 10 to 30% of which will die within one month of diagnosis.[2][11]
  • Among people who have had a DVT, one-half will have long-term complications (post-thrombotic syndrome) such as swelling, pain, discoloration, and scaling in the affected limb.[2][11]

References

  1. ↑ 1.0 1.1 CDC- Deep Vein Thrombosis (DVT) / Pulmonary Embolism (PE) — Blood Clot Forming in a Vein
  2. ↑ 2.0 2.1 2.2 2.3 2.4 Beckman MG, Hooper WC, Critchley SE, Ortel TL (2010). “Venous thromboembolism: a public health concern”. Am J Prev Med. 38 (4 Suppl): S495–501. doi:10.1016/j.amepre.2009.12.017. PMID 20331949.
  3. ↑ 3.0 3.1 3.2 3.3 White RH (2003). “The epidemiology of venous thromboembolism”. Circulation. 107 (23 Suppl 1): I4–8. doi:10.1161/01.CIR.0000078468.11849.66. PMID 12814979. Unknown parameter |month= ignored (help)
  4. ↑ 4.0 4.1 4.2 4.3 Cushman M, Tsai AW, White RH, Heckbert SR, Rosamond WD, Enright P; et al. (2004). “Deep vein thrombosis and pulmonary embolism in two cohorts: the longitudinal investigation of thromboembolism etiology”. Am J Med. 117 (1): 19–25. doi:10.1016/j.amjmed.2004.01.018. PMID 15210384.
  5. ↑ Silverstein MD, Heit JA, Mohr DN, Petterson TM, O’Fallon WM, Melton LJ (1998). “Trends in the incidence of deep vein thrombosis and pulmonary embolism: a 25-year population-based study”. Arch. Intern. Med. 158 (6): 585–93. PMID 9521222. Unknown parameter |month= ignored (help)
  6. ↑ Kniffin WD, Baron JA, Barrett J, Birkmeyer JD, Anderson FA (1994). “The epidemiology of diagnosed pulmonary embolism and deep venous thrombosis in the elderly”. Arch. Intern. Med. 154 (8): 861–6. PMID 8154949. Unknown parameter |month= ignored (help)
  7. ↑ “Venous Thromboembolism in Adult Hospitalizations — United States, 2007–2009”. Retrieved 2012-10-06.
  8. ↑ Ridker PM, Miletich JP, Hennekens CH, Buring JE (1997). “Ethnic distribution of factor V Leiden in 4047 men and women. Implications for venous thromboembolism screening”. JAMA. 277 (16): 1305–7. PMID 9109469.
  9. ↑ Gregg JP, Yamane AJ, Grody WW (1997). “Prevalence of the factor V-Leiden mutation in four distinct American ethnic populations”. Am J Med Genet. 73 (3): 334–6. PMID 9415695.
  10. ↑ 10.0 10.1 10.2 10.3 10.4 [1] Hussain R. Yusuf, MD, James Tsai, MD, Hani K. Atrash, MD, Sheree Boulet, DrPH, Scott D. Grosse, PhD, Div of Blood Disorders, National Center on Birth Defects and Developmental Disabilities, CDC. Venous Thromboembolism in Adult Hospitalizations — United States, 2007–2009
  11. ↑ 11.0 11.1 11.2 CDC- Deep Vein Thrombosis (DVT) / Pulmonary Embolism (PE) — Blood Clot Forming in a Vein
  12. ↑ Heit JA, Mohr DN, Silverstein MD, Petterson TM, O’Fallon WM, Melton LJ (2000). “Predictors of recurrence after deep vein thrombosis and pulmonary embolism: a population-based cohort study”. Arch. Intern. Med. 160 (6): 761–8. PMID 10737275. Unknown parameter |month= ignored (help)

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Risk Factors

Risk Factors

Editor(s)-In-Chief: The APEX Trial Investigators, C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Cafer Zorkun, M.D., Ph.D. [2] Kashish Goel, M.D.; Assistant Editor(s)-In-Chief: Justine Cadet; Rim Halaby, M.D. [3]

Overview

Venous thromboembolism (VTE) consists of deep vein thrombosis (DVT), pulmonary embolism (PE), or both. In these chapters on VTE, the word risk factors refers to those epidemiologic and genetic variables that expose someone to a higher risk of developing venous thrombosis. The word triggers refer to those factors in the patients immediate history or environment that may have led to the occurrence of the venous thrombosis. The risk factors for VTE are a constellation of predisposing conditions which stem from the three principles of Virchow’s triad: stasis of the blood flow, damage to the vascular endothelial cells, and hypercoagulability. The risk factors for VTE can be classified as temporary, modifiable and non-modifiable. It is suggested that venous thrombosis also shares risk factors with arterial thrombosis, such as obesity, hypertension, smoking, and diabetes mellitus.[1]

Risk Factors

Shown below is a list of predisposing factors to VTE.[2][3] The risk factors are classified as moderate or weak depending on how strongly they predispose for a VTE.

Moderate risk factors Weak risk factors

❑ Chemotherapy
❑ Chronic heart failure
❑ Respiratory failure
❑ Hormone replacement therapy
❑ Cancer
❑ Oral contraceptive pills
❑ Stroke
❑ Pregnancy
❑ Postpartum
❑ Prior history of VTE
❑ Thrombophilia

❑ Advanced age

❑ Laparoscopic surgery
❑ Prepartum
❑ Obesity
❑ Varicose veins


The risk factors of VTE can be further classified into modifiable, non-modifiable and temporary.

Modifiable Risk Factors

Modifiable risk factors are reversible based upon lifestyle/behavior modification.

Non-Modifiable Risk Factors

Temporary Risk Factors


Other Possible Risk Factors

Other possible factors associated with VTE include:

Courtesy CDC


References

  1. ↑ Goldhaber SZ (2010). “Risk factors for venous thromboembolism”. J Am Coll Cardiol. 56 (1): 1–7. doi:10.1016/j.jacc.2010.01.057. PMID 20620709.
  2. ↑ Anderson FA, Spencer FA (2003). “Risk factors for venous thromboembolism”. Circulation. 107 (23 Suppl 1): I9–16. doi:10.1161/01.CIR.0000078469.07362.E6. PMID 12814980.
  3. ↑ Torbicki A, Perrier A, Konstantinides S, Agnelli G, Galiè N, Pruszczyk P; et al. (2008). “Guidelines on the diagnosis and management of acute pulmonary embolism: the Task Force for the Diagnosis and Management of Acute Pulmonary Embolism of the European Society of Cardiology (ESC)”. Eur Heart J. 29 (18): 2276–315. doi:10.1093/eurheartj/ehn310. PMID 18757870.
  4. ↑ 4.0 4.1 Holst AG, Jensen G, Prescott E (2010). “Risk factors for venous thromboembolism: results from the Copenhagen City Heart Study”. Circulation. 121 (17): 1896–903. doi:10.1161/CIRCULATIONAHA.109.921460. PMID 20404252.
  5. ↑ Vayá A, Martínez-Triguero ML, España F, Todolí JA, Bonet E, Corella D (2011). “The metabolic syndrome and its individual components: its association with venous thromboembolism in a Mediterranean population”. Metab Syndr Relat Disord. 9 (3): 197–201. doi:10.1089/met.2010.0117. PMID 21352080.
  6. ↑ Eichinger S, Hron G, Bialonczyk C, Hirschl M, Minar E, Wagner O; et al. (2008). “Overweight, obesity, and the risk of recurrent venous thromboembolism”. Arch Intern Med. 168 (15): 1678–83. doi:10.1001/archinte.168.15.1678. PMID 18695082.
  7. ↑ Pomp ER, Rosendaal FR, Doggen CJ (2008). “Smoking increases the risk of venous thrombosis and acts synergistically with oral contraceptive use”. Am J Hematol. 83 (2): 97–102. doi:10.1002/ajh.21059. PMID 17726684.
  8. ↑ den Heijer M, Koster T, Blom HJ, Bos GM, Briet E, Reitsma PH; et al. (1996). “Hyperhomocysteinemia as a risk factor for deep-vein thrombosis”. N Engl J Med. 334 (12): 759–62. doi:10.1056/NEJM199603213341203. PMID 8592549.
  9. ↑ Steffen LM, Folsom AR, Cushman M, Jacobs DR, Rosamond WD (2007). “Greater fish, fruit, and vegetable intakes are related to lower incidence of [[venous thromboembolism]]: the Longitudinal Investigation of Thromboembolism Etiology”. Circulation. 115 (2): 188–95. doi:10.1161/CIRCULATIONAHA.106.641688. PMID 17179018. URL–wikilink conflict (help)
  10. ↑ Rosengren A, Fredén M, Hansson PO, Wilhelmsen L, Wedel H, Eriksson H (2008). “Psychosocial factors and [[venous thromboembolism]]: a long-term follow-up study of Swedish men”. J Thromb Haemost. 6 (4): 558–64. doi:10.1111/j.1538-7836.2007.02857.x. PMID 18045241. URL–wikilink conflict (help)
  11. ↑ Ageno W, Becattini C, Brighton T, Selby R, Kamphuisen PW (2008). “Cardiovascular risk factors and venous thromboembolism: a meta-analysis”. Circulation. 117 (1): 93–102. doi:10.1161/CIRCULATIONAHA.107.709204. PMID 18086925.
  12. ↑ McColl MD, Tait RC, Greer IA, Walker ID (2001). “Injecting drug use is a risk factor for [[deep vein thrombosis]] in women in Glasgow”. Br J Haematol. 112 (3): 641–3. PMID 11260066. URL–wikilink conflict (help)
  13. ↑ Naik RP, Streiff MB, Haywood C, Nelson JA, Lanzkron S (2013). “Venous thromboembolism in adults with sickle cell disease: a serious and under-recognized complication”. Am J Med. 126 (5): 443–9. doi:10.1016/j.amjmed.2012.12.016. PMC 3627211. PMID 23582935.
  14. ↑ Koutroumpakis EI, Tsiolakidou G, Koutroubakis IE (2013). “Risk of venous thromboembolism in patients with inflammatory bowel disease”. Semin Thromb Hemost. 39 (5): 461–8. doi:10.1055/s-0033-1343886. PMID 23629820.
  15. ↑ Jönsson AK, Spigset O, Hägg S (2012). “Venous thromboembolism in recipients of antipsychotics: incidence, mechanisms and management”. CNS Drugs. 26 (8): 649–62. doi:10.2165/11633920-000000000-00000. PMID 22731933.
  16. ↑ Ho KM, Yip CB, Duff O (2012). “Reactive thrombocytosis and risk of subsequent venous thromboembolism: a cohort study”. J Thromb Haemost. 10 (9): 1768–74. doi:10.1111/j.1538-7836.2012.04846.x. PMID 22784217.
  17. ↑ Müller-Bühl U, Leutgeb R, Engeser P, Achankeng EN, Szecsenyi J, Laux G (2012). “Varicose veins are a risk factor for deep venous thrombosis in general practice patients”. Vasa. 41 (5): 360–5. doi:10.1024/0301-1526/a000222. PMID 22915533.
  18. ↑ Königsbrügge O, Lötsch F, Reitter EM, Brodowicz T, Zielinski C, Pabinger I; et al. (2013). “Presence of varicose veins in cancer patients increases the risk for occurrence of venous thromboembolism”. J Thromb Haemost. 11 (11): 1993–2000. doi:10.1111/jth.12408. PMID 24112869.

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Triggers

Triggers

Editor(s)-In-Chief: The APEX Trial Investigators, C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Cafer Zorkun, M.D., Ph.D. [2] Kashish Goel, M.D.; Assistant Editor(s)-In-Chief: Justine Cadet; Rim Halaby, M.D. [3]

Overview

Venous thromboembolism (VTE) consists of deep vein thrombosis (DVT), pulmonary embolism (PE), or both. In these chapters on VTE, the word risk factors refers to those epidemiologic and genetic variables that expose someone to a higher risk of developing venous thrombosis. The word triggers refer to those factors in the patients immediate history or environment that may have led to the occurrence of the venous thrombosis. The triggers of VTE include injury to a deep vein from surgery, a fracture, or other trauma, especially a paralytic spinal cord injury.[1] Another trigger for VTE is prolonged immobilization that causes stasis in the deep veins which may occur after surgery, prolonged bed-rest, or prolonged seating during travel.

Triggers

Shown below is a list of triggers of VTE.[1][2] The triggers are classified as strong, moderate, or weak depending on how strongly they predispose for a VTE.

Strong triggers Moderate triggers Weak triggers
❑ Bone fracture (hip or leg)

❑ Hip replacement surgery
❑ Knee replacement surgery
❑ Major general surgery
❑ Significant trauma
❑ Spinal cord injury

 ❑ Athroscopic knee surgery

❑ Central venous lines
❑ Chemotherapy

 ❑ Bed rest for more than 3 days

❑ Prolonged car or air travel
❑ Laparoscopic surgery
❑ Prepartum

Triggers for Upper Extremity DVT

Shown below is a list of triggers for upper extremity DVT:[3]

References

  1. ↑ 1.0 1.1 Anderson FA, Spencer FA (2003). “Risk factors for venous thromboembolism”. Circulation. 107 (23 Suppl 1): I9–16. doi:10.1161/01.CIR.0000078469.07362.E6. PMID 12814980. Unknown parameter |month= ignored (help)
  2. ↑ Torbicki A, Perrier A, Konstantinides S, Agnelli G, Galiè N, Pruszczyk P; et al. (2008). “Guidelines on the diagnosis and management of acute pulmonary embolism: the Task Force for the Diagnosis and Management of Acute Pulmonary Embolism of the European Society of Cardiology (ESC)”. Eur Heart J. 29 (18): 2276–315. doi:10.1093/eurheartj/ehn310. PMID 18757870.
  3. ↑ Kucher N (2011). “Clinical practice. Deep-vein thrombosis of the upper extremities”. N Engl J Med. 364 (9): 861–9. doi:10.1056/NEJMcp1008740. PMID 21366477.

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Screening

Screening

Editor(s)-In-Chief: The APEX Trial Investigators, C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Cafer Zorkun, M.D., Ph.D. [2] Kashish Goel, M.D.; Assistant Editor(s)-In-Chief: Justine Cadet; Rim Halaby, M.D. [3]

Overview

In spite of identifying patients at increased risk of venous thromboembolism (VTE), there is no clear clinical value for screening the general population. Screening for asymptomatic deep vein thrombosis (DVT) with venous compression ultrasound is not recommended for critically ill medical patients,[1] patients undergoing general surgery[2] or orthopedic surgeries.[3]

References

  1. ↑ Kahn SR, Lim W, Dunn AS, Cushman M, Dentali F, Akl EA; et al. (2012). “Prevention of VTE in nonsurgical patients: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines”. Chest. 141 (2 Suppl): e195S–226S. doi:10.1378/chest.11-2296. PMC 3278052. PMID 22315261.
  2. ↑ Gould MK, Garcia DA, Wren SM, Karanicolas PJ, Arcelus JI, Heit JA; et al. (2012). “Prevention of VTE in nonorthopedic surgical patients: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines”. Chest. 141 (2 Suppl): e227S–77S. doi:10.1378/chest.11-2297. PMC 3278061. PMID 22315263.
  3. ↑ Falck-Ytter Y, Francis CW, Johanson NA, Curley C, Dahl OE, Schulman S; et al. (2012). “Prevention of VTE in orthopedic surgery patients: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines”. Chest. 141 (2 Suppl): e278S–325S. doi:10.1378/chest.11-2404. PMC 3278063. PMID 22315265.

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Natural History, Complications and Prognosis

Natural History, Complications and Prognosis

Editor(s)-In-Chief: The APEX Trial Investigators, C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Cafer Zorkun, M.D., Ph.D. [2] Kashish Goel, M.D.; Assistant Editor(s)-In-Chief: Justine Cadet

Overview

Thrombus formation typically begins in the calf veins and naturally progresses to the proximal veins and ultimately, breaks free from the site formation and travels to the pulmonary artery where it is called a pulmonary embolism. In many cases, patients with a thrombus can be asymptomatic until it progresses into the proximal veins.

Natural History

  • Many patients with a deep vein thrombosis (DVT) originating in the calf veins are asymptomatic until proximal vein involvement.[1] However, even assymptomatic DVTs are associated with increased risk of death[2].
  • About half of all calf DVTs resolve spontaneously, without intervention.[1]
  • One-sixth of all calf DVTs progress to involvement with the proximal veins.[1]
  • Typical onset of thrombus formation may occur during the intraoperative period though there is a potential latent onset up to many months after the initial surgery.[1]
  • Surgeries characteristically responsible for thrombus formation include:
  • Knee replacement surgery is associated with twice the frequency of asymptomatic onset.[1]
  • Without treatment, one-fourth to one-third of symptomatic, isolated distal thrombi in the deep veins involve proximal veins.[1]
    • Patients with isolated calf DVT treated with five days of heparin therapy without a tandem oral anticoagulant therapy were at highest risk for recurrent or extension of DVT within three months of follow-up.[1]
  • Patients with untreated DVT have the potential to develop:
  • Mortality rates associated with venous thrombosis can be very high.
    • In one study, 6% of patients with DVT died within one month of diagnosis.[3]
    • Other research suggests that approximately one-fourth of all patients die within one year of venous thrombosis onset.[1]
    • Patients presenting with a venous thrombosis consistently have higher in-hospital mortality rates.[1]

Rule of 30’s

  • 30% will die in 30 days.
  • 30% will have recurrence in 10 years. The actual number at 10 years has been reported to be 36%[4]
  • 30% will develop post phlebitic syndrome.

Complications

Venous thrombosis may lead to any of the following major complications:

  • Recurrence may occur unevenly across the sexes; with men being almost four times more likely than women for a venous thrombosis recurrence.[5]
  • Major bleeding due to anticoagulation
  • Death – Proximal vein thrombosis is responsible for more than ninety percent of acute pulmonary emboli. Acute PE is ultimately associated with a high mortality if not treated promptly. [6]

Other complications include:

The rate of complications in lower extremity DVT is higher from that in upper extremity DVT. Shown below is a table summarizing the differences in the rate of occurrence of complications.[8]

Complications Upper extremity DVT Lower extremity DVT
Pulmonary embolism 6% 15-32%
Recurrence of DVT 2-5% 10%
Post thrombotic syndrome 5% 56%

Prognosis

Probability of recurrence can be estimated with the HERDOO2 rule:[9]

  • Hyperpigmentation
  • Edema
  • Redness in either leg
  • D-dimer level ≥250 μg/L
  • Obesity with body mass index ≥30
  • Older age, ≥65 years

Per the authors, “Women with a first unprovoked VTE event and none or one of the HERDOO2 criteria have a low risk of recurrent VTE and can safely discontinue anticoagulants after completing short term treatment.”[9]

References

  1. ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 1.8 Kearon C (2003). “Natural history of venous thromboembolism”. Circulation. 107 (23 Suppl 1): I22–30. doi:10.1161/01.CIR.0000078464.82671.78. PMID 12814982. Unknown parameter |month= ignored (help)
  2. ↑ Kalayci A, Gibson CM, Chi G, Yee MK, Korjian S, Datta S; et al. (2018). “Asymptomatic Deep Vein Thrombosis is Associated with an Increased Risk of Death: Insights from the APEX Trial”. Thromb Haemost. 118 (12): 2046–2052. doi:10.1055/s-0038-1675606. PMID 30419597.
  3. ↑ White RH (2003). “The epidemiology of venous thromboembolism”. Circulation. 107 (23 Suppl 1): I4–8. doi:10.1161/01.CIR.0000078468.11849.66. PMID 12814979.
  4. ↑ Khan F, Rahman A, Carrier M, Kearon C, Weitz JI, Schulman S; et al. (2019). “Long term risk of symptomatic recurrent venous thromboembolism after discontinuation of anticoagulant treatment for first unprovoked venous thromboembolism event: systematic review and meta-analysis”. BMJ. 366: l4363. doi:10.1136/bmj.l4363. PMID 31340984.
  5. ↑ Kyrle PA, Minar E, Bialonczyk C, Hirschl M, Weltermann A, Eichinger S (2004). “The risk of recurrent venous thromboembolism in men and women”. N Engl J Med. 350 (25): 2558–63. doi:10.1056/NEJMoa032959. PMID 15201412. Review in: ACP J Club. 2004 Nov-Dec;141(3):78
  6. ↑ Galanaud JP, Sevestre-Pietri MA, Bosson JL, Laroche JP, Righini M, Brisot D, Boge G, van Kien AK, Gattolliat O, Bettarel-Binon C, Gris JC, Genty C, Quere I (2009). “Comparative study on risk factors and early outcome of symptomatic distal versus proximal deep vein thrombosis: results from the OPTIMEV study”. Thromb. Haemost. 102 (3): 493–500. doi:10.1160/TH09-01-0053. PMID 19718469. Retrieved 2011-12-14. Unknown parameter |month= ignored (help)
  7. ↑ Kahn SR, Ducruet T, Lamping DL, Arsenault L, Miron MJ, Roussin A; et al. (2005). “Prospective evaluation of health-related quality of life in patients with deep venous thrombosis”. Arch Intern Med. 165 (10): 1173–8. doi:10.1001/archinte.165.10.1173. PMID 15911732.
  8. ↑ Kucher N (2011). “Clinical practice. Deep-vein thrombosis of the upper extremities”. N Engl J Med. 364 (9): 861–9. doi:10.1056/NEJMcp1008740. PMID 21366477.
  9. ↑ 9.0 9.1 Rodger MA, Le Gal G, Anderson DR, Schmidt J, Pernod G, Kahn SR; et al. (2017). “Validating the HERDOO2 rule to guide treatment duration for women with unprovoked venous thrombosis: multinational prospective cohort management study”. BMJ. 356: j1065. doi:10.1136/bmj.j1065. PMID 28314711.

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Diagnosis

Diagnosis

Diagnostic Approach | Assessment of Clinical Probability and Risk Scores | Assessment of Probability of Subsequent VTE and Risk Scores | History and Symptoms | Physical Examination | Laboratory Findings | Ultrasound | Venography | CT | MRI | Other Imaging Findings

Treatment

Treatment

Treatment Approach | Medical Therapy | Compression stockings | IVC filter | Invasive Therapy | Surgery | Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2] Ujjwal Rastogi, MBBS [3]

Overview

The primary objectives of treatment of DVT are to control the following:

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Special Scenarios

Upper Extremity DVT | Recurrence | Pregnancy

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Trials

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