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Edema and Deep Venous Thrombosis

Deep Venous Thrombosis (DVT) 

Related Terms:  Blood clots, DVT, Venous Stasis, leg swelling, deep vein thrombophlebitis, pulmonary embolism, deep vein blood clots, venous thrombosis, leg edema, Homans sign, lymphedema fibrosis, sepsis, nephrotic syndrome, congestive heart failure, stroke, acute myocardial infarction, heart attack, lymphedema


Medical condition that affects mainly the lower legs and thigh and involves the formation of a blood clot.  The clot cuts off blood circulation and can lead to several serious complications.  The signs and symptoms of the condition will vary depending on the intensity or size of the clot.

Risk factors:

There are a number of general risk factors associated with DVT.  These include age, immobilization for longer than three days, pregnancy and the post-partum period, extensive surgical procedure within the previous month.

In addition to the general risk factors, there are important medical based risk factors as well.  These include cancer, sepsis, nephrotic syndrome, congestive heart failure (CHF), fibrosis in lymphedema limbs, stroke, acute myocardial  infarction (AMI - heart attack).

Other causes include trauma injury, inherited hematologic disordes, and drugs and medications.


Edema of the affected limb, pulmonary embolism, post-thrombotic syndrome, hemorhagic complications from anticoagulants and blood thinners, chronic venous insufficiency, soft-tissue ischemia, risk of cellulitis from the edema


Homans sign (Slight pain at the back of the knee or calf when the ankle is slowly and gently dorsiflexed (with the knee bent), indicative of incipient or established thrombosis in the veins of the leg.)

Unexplained sharp leg pain in only one leg, sudden edema in only one leg, leg tenderness, increased warmth in the affected leg, changes in the coloration (red) of the affected leg, venous distension (often visible or noticeable by touch), 


Diagnostic radiological tests are standard protocol for the diagnosis and assessment of deep venous thrombosis.

These tests include contrast venography, duplex ultrasonography, impedance  plethysomography and MRI.


The main treatment for deep venous thrombosis has been the use of the blood thinner Heparin. This is started immediately, often through inter-venous application.  Within a few days another anticoagulant drug called warfarin is administered. Heparin and warfarin are used together for several days, then warfarin is continued, often for months.

After the resolution of the clot, standard patient treatment protocol will focus on the initial cause of the thrombosis.


The patient recovery expectation is excellent as most thrombosis disappear without difficulty.  However, they may reoccur therefore it is critical that the patient has long term follow up.  It may also be necessary to continue preventative drug therapy for an extended period of time.


Deep Venous Thrombosis in Lymphedema

Venous thrombosis is a serious and life threatening potential complication of lymphedema, especially in stages 2 and 3 where the fibrosis is extensive. (See Lymphedema Stages)

Simply defined venous thrombosis or blood clot is where there is a rapid coagulation of blood due to either sluggish blood flow or from a cut off of blood flow.

A blood clot will be immediately quite painful, can cause a profound change in the coloration of the limb to dark pink or purplish, and cause a localized buldge or increased edema.

The three biggest causes of these clots are fibrosis and its affect on the vascular system and blood flow, infections such a recurrent cellulitis and lymphangitis, and cut off of circulation in long airlines flights or even automobile trips.

When you travel you should from time to time get up and "stretch" your legs allowing the circulation to move.

Prevention of Deep Venous Thrombosis in Lymphedema 

Obtain systematic and consistent decongestive therapy to decrease, and control the lymphedema.  This will help prevent fibrosis which is a prime factor in deep venous thrombosis.

When traveling any distance, move around, walk, stretch.  While you are sitting move your legs around from time to time.

Undertake proper skin care to prevent cracks, wounds, peeling or drying out of the skin. This will help prevent cellulitis, another factor in DVT.

Depending on accompanying medical conditions, if you do have cellulitis, lymphangitis or any other type of infection and especially if you are bed ridden, discuss with your physician the possible use of heparin or another blood thinner to temporarily decrease the risk.

Follow a sensible and healthy diet that will help prevent cardiovascular difficulties.  This is good common sense even if you do not have lymphedema.

Deep Venous Thrombosis - Airline Traveling Tips    

Wear loose, comfortable clothing and avoid tight stockings.   

Drink enough water or non-alcoholic beverages during flights  (2 dl per hour).   

Be careful that the space for the legs in front of the seat is not blocked by hand luggage.   

Avoid sleeping in an uncomfortable position and be careful with sleeping drugs.   

Limiting the length of time you sit still can reduce the possibility of circulatory problems, particularly traveler's thrombosis. Simple exercises (stretching and moving arms and legs and ankles) can help. 

The risk of thrombosis is elevated for persons with a history of thrombosis and pulmonary embolism. These people should consult their doctor in advance of a flight. She/he will instruct them concerning the use of elasticised low-compression stockings and/or the need of specific medication (low molecular heparins).  

Talk with your healthcare provider about taking aspirin for its blood-thinning properties. 

A short walk at transit stations and after landing to stimulate circulation is recommended           

Treatment of Deep Venous Thrombosis in Lymphedema 

The main treatment for DVT in lymphedema patients will be the same as for the general population.  This has traditionally involved the usage of blood thinners, typically heparin.  This drug acts as not just a thinner, but also an anticoagulant.  Several days therapy with heparin is started another drug called Warfarin is used. Whereas this drug usually takes several days to become effective both are used for a short period of time.

Deep Venous Thrombosis Warning

Due to the potential complication of deep venous thrombosis (blood clots) in lymphedema below are some info articles on this.

If you have sudden unexplained swelling (especially of the legs)
you must let your doctor know as it could be caused from a blood clot
which untreated can be fatal.

Tips on Treament of Lymphedema with Deep Venous Thrombosis


If you recently had or currently have a blood clot, DVT, thrombosis, in other words a vascular blockage in any form, you must not have lymphedema massage physiotherapy.  This is critical as the massage could potentially cause the clot to break loose and travel to your heart or lungs.

Compression garments - It is also important to remember that the compression strength for DVT versus lymphedema is different.  You will need to wear the compression hosiery for DVT, which is the most life threatening condition.

Compression Pneumatics Pumps - Under no circumstance should any pneumatic compression device be used if you have DVT, or a clot of any type.


Deep Venous Thrombosis

Gisele de Azevedo Prazeres


Three tests have good accuracy for diagnosing Deep Vein Thrombosis (DVT) in symptomatic patients : venography, impedance plethismography (IPG) and duplex venous ultrasound (B - mode imaging ). In most patients with clinically suspected venous thrombosis, venous ultrasound is the diagnostic method of choice.

In addition, the simpli -red -D-dimer test, which is performed on blood obtained by finger prick at the patient’s side and which has high sensitivity and moderate specificity, shows considerable promise as a test to rule out venous thrombosis. The D-dimer test is often false-positive after surgery or trauma, thereby limiting its value in these clinical situations

Computed Tomography (CT) and Magnetic Resonance Imaging (MRI) are also useful in some circumstances (see TABLE 1 ). Venography, although invasive, is the “gold standard” diagnostic procedure, and the best noninvasive substitute for venography is duplex ultrasound.


Exam Main use
Venography Considered “gold standard”. Used when other
test results are not conclusive
Duplex ultrasound Most sensitive for thrombosis above the knee
MRI, Contrast CT Most sensitive for thrombosis of pelvic veins
IPG Good alternative to duplex ultrasound, but
less specific/sensitive

Differential Diagnosis

There are many other conditions that cause localized pain or edema in the lower extremities, and may be confused with DVT. These differential diagnosis include: ruptured popliteal synovial membrane or cyst (Baker’cyst), ruptured calf muscles or tendons, a severe muscle cramp, cellulitis and lymphedema. The examiner should be attempt to the patient’s history and physical signs, because in the situations described above some signs of DVT may be present but not all of them, and in each one of these conditions the management is different.


Pulmonary embolism (PE ) is a serious and frequent complication of DVT. Pulmonary emboli are detected by perfusion lung scanning in approximately 50% of patients with documented DVT, and asymptomatic venous thrombosis is found in 70% of patients with confirmed clinically symptomatic PE. Although DVT may begin frequently in the veins of the calf, it is only when the thrombosis extends above the knee that serious pulmonary embolism occurs.

Postthrombotic syndrome occurs in about 25% of cases. It is caused by venous hypertension, which occurs as a consequence of recanalization of major venous thrombi leading to patent but scarred and incompetent valves, or less frequently, persistent outflow obstruction produced by large proximal vein thrombi. This high pressure results in edema and impaired viability of subcutaneous tissues and, in its most severe forms, ulceration of venous origin.

In patients with extensive thrombosis involving the ileofemoral veins, swelling may never disappear, while in patients with less severe proximal vein thrombosis, swelling may subside after the initial event but may return in the next few years. Other manifestations of postthrombotic syndrome are pain in the calf relieved by rest and elevation of the leg, pigmentation and induration around the ankle and the lower third of the leg, and, less commonly venous claudication, a bursting calf pain that occurs during exercise (mainly in ileofemoral thrombosis).

The diagnosis of postthrombotic syndrome is sometimes obvious on clinical grounds if the symptoms are gradual in onset. However, patients can have subacute symptoms of leg pain and swelling, which may mimic acute recurrence of DVT. Although these symptoms are usually superimposed on a background of chronic pain and swelling, it may be difficult to exclude acute recurrence on clinical grounds alone, and a diagnosis of postthrombotic syndrome as the cause of the patient’ symptoms can be made only after acute recurrent venous thrombosis has been excluded (the best exam to do this is MRI ).


As soon as the diagnosis of DVT has been made, treatment (which consists of anticoagulation ) should begin, in the way to prevent local extension of the thrombus, prevent the thrombus from embolizing, and, in certain clinical circumstances, accelerate fibrinolysis. Full anticoagulation is the best treatment for DVT. Heparin is preferred to initiate treatment because of its immediate action, whereas warfarin-type drugs may not become fully effective for a considerable period of time. See TABLE 2 with the guidelines for use of anticoagulants in the treatment of DVT. Furthermore, patients should be encourage to use graduated compression stockings after the acute episode of DVT to prevent postthrombotic syndrome.


Treatment of DVT
Bolus dose of heparin: 5000-10000 U EV
Initial maintenance dose of heparin: 32000 U EV per 24h by continuous
infusion or 17000 U subcutaneously to be repeated after adjustment at 12h
Adjust dose of heparin at 6h according to normogram. Maintain aPTT
2 times the control
Repeat aPTT 6 times every hour until in therapeutic range and then
daily (see nomogram)
Start warfarin 10mg at 24h and 10mg next day.
Overlap heparin and warfarin for at least 4 days
Perform PT daily and adjust warfarin dose to maintain INR at 2.0-3.0
Continue heparin for a minimum of 5 days, then stop if INR has been in
therapeutic range for at least 2 consecutive days.
Continue warfarin for 3 months and monitor PT daily until in therapeutic
range, then 3 times during first week, twice weekly for 2 weeks , or until
dose response is stable, and then every 2 weeks
Obtain pretreatment hemoglobin level, platelet count, PT, and aPTT.
Repeat platelet count daily until heparin stopped.
aPtt= activated Partial Thromboplastin Time;PT= Prothrombin
time; INR= International Normalized Ratio


The most effective way of reducing death from PE and morbidity from postthrombotic syndrome is to institute primary prophylaxis in patients at risk for venous thromboembolism (VTE). Safe and effective forms of prophylaxis are available for patients at high risk, and primary prophylaxis is cost-effective.

Prophylaxis is achieved by either modulating activation of blood coagulation or preventing venous stasis The following prophylactic approaches are of proven value: low dose subcutaneous heparin, intermittent pneumatic compression of legs, oral anticoagulants, adjusted doses of subcutaneous heparin, (low doses which means 5000u every 12 hours), graduated compression stockings, and LMWH (low molecular weigh heparin). Antiplatelet agents such as aspirin are less effective for preventing VTE. See TABLE 3 with some clinical situations of risk for VTE and their suitable prophylaxis

Table 3

Risk for DVT Patients Recommendations
Low Risk Hospitalized medical patients without risk factors Ambulatory leg exercises
Surgical patients under age 40, surgery lasting < 30 minutes, no additional risk factors Ambulatory leg exercises
Moderate risk Hospitalized medical patients with one or more risk factors Low-dose heparin
Surgical patients over age 40 having abdominal or thoracic surgery lasting > 30 minutes Low-dose heparin
Neurosurgery or others patients with high bledding risk Intermittent pneumatic compression of legs
High risk Hip fracture Warfarin(low dose regimen)
Hip replacement Warfarin(low dose regimen) or LMWH
Knee replacement Warfarin(low dose regimen) and intermittent pneumatic compression of the legs
Open prostatectomy intermittent pneumatic compression of the legs
Ginecology Malignancy Intermittent


Kontos H.A.: Vascular diseases of the limbs. In: Bennett J.C., Plum F.[eds].Cecil Textbook of Medicine, pp. 353-356. W.B.Saunders Company, 1996
Creager M.A., Dzau V.J.:Vascular Diseases of the Extremities. In: Isselbacher K.L., Braunwald E., Wilson J.D., Martin J.B., Fauci A.S., Kasper D.L. [eds]. Harisson’s Principles of Internal Medicine, pp. 1140-1142. Mc Graw Hill, 1994.
Goldhaber S.Z. : Deep Vein Thrombosis and Pulmonary Embolism. Harvard Medical School - Board Review Course, 1996.
Hirsh J., Hoak J.: Management of Deep Venous Thrombosis and Pulmonary Embolism. In Circulation, 1996; 93: 2212-2245.


Swollen lower limb---1: General assessment and deep vein thrombosis

W Peter Gorman Karl R Davis Richard Donnelly 

The most common cause of leg swelling is oedema, but expansion of all or part of a limb may be due to an increase in any tissue component (muscle, fat, blood, etc). A correct diagnosis requires consideration of whether the swelling is acute or chronic, symmetrical or asymmetrical, localised or generalised, and congenital or acquired. Chronic swelling, particularly if asymmetrical, is usually a sign of chronic oedema arising from venous or lymphatic disease, whereas symmetrical lower limb swelling suggests a systemic or more central cause of oedema, such as heart failure or nephrotic syndrome. Oedema develops when the rate of capillary filtration (lymph formation) exceeds lymphatic drainage, either because of increased capillary filtration, inadequate lymphatic flow, or both. Extracellular fluid volume is controlled prinicpally by the lymphatic system, which normally compensates for increases in capillary filtration. Most oedemas arise because filtration overwhelms the lymph drainage system. Increased capillary filtration may occur because of raised venous pressure, hypoalbuminaemia, or increased capillary permeability due to local inflammation. The two main causes of a swollen lower limb are deep vein thrombosis and lymphoedema (a failure of the lymph drainage system). This article concentrates on deep vein thrombosis and next week's article on lymphoedema.

Causes of swelling of lower limb


Congenital vascular abnormalities

Venous disease Lymphoedema Other

Deep vein thrombosis

Thrombosis usually develops as a result of venous stasis or slow flowing blood around venous valve sinuses; extension of the primary thrombus occurs within or between the deep and superficial veins of the leg and the propagating clot causes venous obstruction, damage to valves, and possible thromboembolism. Deep vein thrombosis is often asymptomatic.

Various clinical features suggest deep vein thrombosis, but the findings of physical examination alone are notoriously unreliable. Deep vein thrombosis is confirmed in only one out of every three cases suspected clinically. Confirmation of a suspected deep vein thrombosis requires use of one or more investigations, and the confirmation rate rises with the number of clinical risk factors. Identification of an underlying cause, if any, will guide both the treatment and the approach to secondary prevention

The standard investigation is contrast venography, but this invasive procedure is painful, often technically difficult and time consuming, and occasionally complicated by thrombosis and extravasation of contrast. Recent developments in non-invasive testing mean that venography is now unnecessary in most cases, particularly in suspected first proximal vein thrombosis. 

The accuracy of non-invasive techniques varies with the clinical circumstances. For example, compression ultrasonography and impedance plethysmography are accurate for detecting symptomatic proximal (ileofemoral) deep vein thrombosis, but both techniques are less satisfactory in asymptomatic patients and for detecting distal (calf vein) thrombosis. Compression ultrasonography has become the preferred first line investigation (see BMJ 2000;320:698-701).

Imaging techniques are generally much less satisfactory in patients with suspected recurrent deep vein thrombosis, when confirmation of the diagnosis requires evidence of new thrombus formation---for example, the appearance of a new non-compressible venous segment on ultrasonography or a new intraluminal filling defect on venography. 

Measurement of circulating D-dimer concentrations (a byproduct of fibrin production) is a useful adjunct to ultrasonography, with 98% sensitivity for deep vein thrombosis and a high negative predictive value. The sensitivity of the test is lower for smaller calf vein thrombi. However D-dimer concentrations rise as a non-specific response to concomitant illness, not just thrombosis, so D-dimer testing can be misleading in patients admitted to hospital for other reasons.

A combination of diagnostic approaches---for example, compression ultrasonography coupled with clinical pretest probability scoring or D-dimer measurements, or both, gives better diagnostic accuracy than any single investigation. Lensing et al have recently shown that the combination of compression ultrasonography and D-dimer measurement is an efficient diagnostic approach, with a rate of subsequent thromboembolism less than 1% in patients with false negative results who were not treated with heparin. A robust investigational algorithm has been devised that does not include routine use of venography.

Risk factors for deep vein thrombosis

Clinical features of acute deep vein thrombosis Clinical model to determine pretest probability of deep vein thombosis (3 points=high risk, 1 or 2=moderate, 0=low)
Active cancer (treatment ongoing, or within 6 months, or palliative) 1
Paralysis, paresis or recent plaster immobilisation of the legs 1
Recent immobilisation > 3days or major surgery within 12 weeks requiring general or regional anaesthesia 1
Localised tenderness along the distribution of the deep venous system 1
Entire leg swollen 1
Calf swelling >3 cm than asymptomatic side (measured 10 cm below tibial tuberosity) 1
Pitting oedema confined to the symptomatic leg 1
Collateral superficial veins (non-varicose) 1
Alternative diagnosis equally or more likely than deep vein thrombosis  -2
Absolute risks of venous thrombotic complications in procedures or conditions of low, moderate, and high risk
Risk level
Risk (%)
Deep vein thrombosis
Proximal deep vein thrombosis
Fatal pulmonary embolism
Low <10 <1 0.01 Minor surgery, trauma, or medical illness Major surgery at age < 40 with no other risk factors
Moderate 10-40 1-10 0.1-1 Major surgery with another risk factor Major trauma, medical illness, or burns Emergency caesarean section in labour Minor surgery with previous deep vein thrombosis, pulmonary embolism, or thrombophilia Lower limb paralysis
High 40-80 10-30 1-10 Major pelvic or abdominal surgery for cancer Major surgery, trauma, or illness with previous pulmonary embolish, deep vein thrombosis, or thrombophilia


The main complications of deep vein thrombosis are pulmonary embolism, post-thrombotic syndrome, and recurrence of thrombosis. Proximal thrombi are a major source of morbidity and mortality. Distal thrombi are generally smaller and more difficult to detect non-invasively, and their prognosis and clinical importance are less clear. However, a fifth of untreated newly developing calf vein thrombi extend proximally, and a quarter are associated with long term symptoms of post-thrombotic syndrome; it is therefore appropriate to treat proved significant calf vein thrombosis.


Patients at significantly increased risk of deep vein thrombosis---for example, those having major pelvic or abdominal surgery for cancer or those with a history of pulmonary embolism or deep vein thrombosis who have serious trauma or illness or are having major surgery---should be given prophylaxis. Early mobilisation and graduated compression stockings are effective, and antiplatelet drugs such as aspirin provide additional protection.

Pneumatic compression devices have been proved effective when used perioperatively and in some groups of medical patients. Low dose unfractionated heparin (5000 units two hours before surgery and 8-12 hourly postoperatively) given by subcutaneous injection reduces the rate of postoperative thromboembolism in general surgical patients by 65%, with little increase in the risk of serious bleeding. Low molecular weight heparins are effective and have some advantages over unfractionated heparin, particularly in high risk patients such as those having hip replacement.


Treatment is aimed at reducing symptoms and preventing complications. Elevation of the leg with some flexion at the knee helps reduce swelling, early mobilisation is beneficial, and use of graded compression stockings achieves a 60% reduction in post-thrombotic syndrome.

It is important to establish effective anticoagulation rapidly. Patients are usually given an intial intravenous heparin bolus of 5000 units followed by unfractionated or low molecular weight heparin for at least five days. With unfractionated heparin an intravenous constant infusion and subcutaneaous injection twice daily are equally effective. A heparin algorithm should be used to adjust the dose. The activated partial thromboplastin time should be checked six hourly until the target is reached and then daily to maintain the international normalised ratio at 1.5-2.5. The platelet count should be checked at the start of treatment and on day 5 to exclude thrombocytopenia. Warfarin should be started on day 1, with the dose determined by a warfarin algorithm. The target ratio is 2-3, and heparin can be stopped when the target ratio is maintained for more than 24 hours. 

Patients with deep vein thrombosis who do not need to be in hospital (around 35%) can be treated with subcutaneous low molecular weight heparin in the community. This can be administered subcutaneously once or twice daily. Low molecular weight heparin has the advantages of a slightly lower rate of haemorrhage and thrombocytopenia and more reliable absorption after injection, and anticoagulation monitoring is not required routinely. Warfarin should be started on day 1, and the duration of treatment guided by the risk profile.

Other approaches
Inferior vena cava filters reduce the rate of pulmonary embolism but have no effect on the other complications of deep vein thrombosis. Thrombolysis should be considered in patients with major proximal vein thrombosis and threatened venous infarction. Surgical embolectomy is restricted to life threatening proximal thrombosis where all else has failed.

Anticoagulating doses of heparin are given for deep vein thrombosis in pregnancy. It is essential to confirm the presence of a thrombus objectively. This is usually done by compression ultrasonography (serially if necessary).

Unfractionated heparin or low molecular weight heparin (which has a better risk profile but is not licensed in United Kingdom for this indication) should then be continued throughout the pregnancy and stopped temporarily before delivery. Anticoagulation should be restarted in the puerperium and continued for six weeks to three months. Warfarin is usually contraindicated during pregnancy because it is teratogenic and increases risk of maternal and fetal haemorrhage perinatally. It can be restarted 48 hours after delivery


W Peter Gorman is consultant physician and Karl R Davis is clinical research fellow, Southern Derbyshire Acute Hospitals NHS Trust, Derby.

The ABC of arterial and venous disease is edited by Richard Donnelly, professor of vascular medicine, University of Nottingham and Southern Derbyshire Acute Hospitals NHS Trust ( ) and Nick J M London, professor of surgery, University of Leicester, Leicester ( ). It will be published as a book later this year.


Medical Encyclopedia

Venous blood clot

Venous blood clot

Deep venous thrombosis (DVT) affects mainly the veins in the lower leg and the thigh. It involves the formation of a clot (thrombus) in the larger veins of the area.

Update Date: 3/23/2001

Deep Venous Thrombosis


External Links:


Deep Venous Thrombosis - DVT


Deep Venous Thrombosis


Deep Venous Thrombosis and Thrombophlebitis - Edema

Author: Donald Schreiber, MD, CM, Assistant Professor of Surgery, Stanford University School of Medicine; Research Director, Division of Emergency Medicine, Stanford University Hospital

Donald Schreiber, MD, CM, is a member of the following medical societies: American College of Emergency Physicians


Diagnostic Imaging of Lower Limb Deep Venous Thrombosis

American Academy of Family Physicians


Concorde Deep Venous Thrombosis and Edema Study: prevention with travel stockings



Deep Venous Thrombosis, Lower Extremity

Author: Robert D Bloch, MD, PhD, Assistant Professor, Department of Interventional and Endovascular Therapy, Southwest Washington Medical Center


Deep Vein Thrombosis (Blood Clot in the Leg, DVT)


Low serum iron levels are associated with elevated plasma levels of coagulation factor VIII and pulmonary emboli/deep venous thromboses in replicate cohorts of patients with hereditary haemorrhagic telangiectasia. Dec 2011


Soluble p-selectin, D-dimer, and high-sensitivity C-reactive protein after acutedeep vein thrombosis of the lower limb. Dec 2011


Medical Encyclopedia

Deep venous thrombosis, ileofemoral

Deep venous thrombosis, ileofemoral

This picture shows a red and swollen thigh and leg caused by a blood clot (thrombus) in the deep veins in the groin (ileofemoral veins) which prevents normal return of blood from the leg to the heart.

Update Date: 1/17/2004


Diagnostic Imaging of Lower Limb Deep Venous Thrombosis

Departments of Radiology and Family Medicine
University of Iowa College of Medicine
Iowa City, Iowa

Pathogenesis of Lower Deep Venous Thrombosis

Figure 1
FIGURE 1. Anatomy of the deep venous system of the lower limb, using the nomenclature given in Nomina Anatomica.



















Figure 2

FIGURE 2. Thrombus formation on a venous valve cusp. (A) Normally, blood flow (straight arrows) proceeds through the valve with the formation of eddy currents (curved arrows). (B) A clot nidus may form on the valve cusp in the setting of stasis. (C) The clot may then extend into the venous lumen.


ICD-10 and ICD-9


Phlebitis and thrombophlebitis
Includes: endophlebitis
inflammation, vein
suppurative phlebitis
Use additional external cause code (Chapter XX), if desired, to identify drug, if drug-induced.
Excludes: phlebitis and thrombophlebitis (of):
· complicating:
  · abortion or ectopic or molar pregnancy ( O00-O07 , O08.7 )
  · pregnancy, childbirth and the puerperium ( O22.- , O87.- )
· intracranial and intraspinal, septic or NOS ( G08 )
· intracranial, nonpyogenic ( I67.6 )
· intraspinal, nonpyogenic ( G95.1 )
· portal (vein) ( K75.1 )
postphlebitic syndrome ( I87.0 )
thrombophlebitis migrans ( I82.1 )
I80.0 Phlebitis and thrombophlebitis of superficial vessels of lower extremities
I80.1 Phlebitis and thrombophlebitis of femoral vein
I80.2 Phlebitis and thrombophlebitis of other deep vessels of lower extremities
Deep vein thrombosis NOS
I80.3 Phlebitis and thrombophlebitis of lower extremities, unspecified
Embolism or thrombosis of lower extremity NOS
I80.8 Phlebitis and thrombophlebitis of other sites
I80.9 Phlebitis and thrombophlebitis of unspecified site
I81 Portal vein thrombosis
Portal (vein) obstruction
Excludes: phlebitis of portal vein ( K75.1 )
I81 Portal vein thrombosis
Portal (vein) obstruction
Excludes: phlebitis of portal vein ( K75.1 )
I82 Other venous embolism and thrombosis
Excludes: venous embolism and thrombosis (of):
· cerebral ( I63.6 , I67.6 )
· complicating:
  · abortion or ectopic or molar pregnancy ( O00-O07 , O08.7 )
  · pregnancy, childbirth and the puerperium ( O22.- , O87.- )
· coronary ( I21-I25 )
· intracranial and intraspinal, septic or NOS ( G08 )
· intracranial, nonpyogenic ( I67.6 )
· intraspinal, nonpyogenic ( G95.1 )
· lower extremities ( I80.- )
· mesenteric ( K55.0 )
· portal ( I81 )
· pulmonary ( I26.- )
I82.0 Budd-Chiari syndrome
I82.1 Thrombophlebitis migrans
I82.2 Embolism and thrombosis of vena cava
I82.3 Embolism and thrombosis of renal vein
I82.8 Embolism and thrombosis of other specified veins
I82.9 Embolism and thrombosis of unspecified vein
Embolism of vein NOS
Thrombosis (vein) NOS

2008 ICD-9-CM Diagnosis 453.40

Venous embolism and thrombosis of unspecified deep vessels of lower extremity

  • 453.40 is a specific code that can be used to specify a diagnosis
  • 453.40 contains 4 index entries
  • View the ICD-9-CM Volume 1 453.* hierarchy

453.40 also known as:

  • Deep vein thrombosis NOS


See also:


Edema and Chronic Venous Insufficiency

Edema and Deep Venous Thrombosis

Edema and Reflex Sympathetic Dystrophy/Complex Regional Pain Syndrome

Edema and Venous Pooling


Edema of the Neck

Edema and Nephrotic Syndrome

Edema of the Face


Edema and Diabetes


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