The risk of VTE is increased in pregnancy by about five times because of a more hypercoagulable state, a likely adaptation against fatal postpartum hemorrhage. Additionally, pregnant women with genetic risk factors are subject to a roughly three to 30 times increased risk for VTE. Preventative treatments for pregnancy-related VTE in hypercoagulable women were suggested by the ACCP. Homozygous carriers of factor V Leiden or prothrombin G20210A with a family history of VTE were suggested for antepartum LMWH and either LMWH or a vitamin K antagonist (VKA) for the six weeks following childbirth. Those with another thrombophilia and a family history but no previous VTE were suggested for watchful waiting during pregnancy and LMWH or—for those without protein C or S deficiency—a VKA. Homozygous carriers of factor V Leiden or prothrombin G20210A with no personal or family history of VTE were suggested for watchful waiting during pregnancy and LMWH or a VKA for six weeks after childbirth. Those with another thrombophilia but no family or personal history of VTE were suggested for watchful waiting only. Warfarin, a common VKA, can cause harm to the fetus and is not used for VTE prevention during pregnancy.

The 2012 ACCP guidelines offered weak recommendations. For at-risk long-haul travelers—those with "previous VTE, recent surgery or trauma, active malignancy, pregnancy, estrogen use, advanced age, limited mobility, severe obesity, or known thrombophilic disorder"—suggestions included calf exercises, frequent walking, and aisle seating in airplanes to ease walking. The use of graduated compression stockings that fit below the knee and give 15–30 mm Hg of pressure to the ankle was suggested, while aspirin or anticoagulants were not. Compression stockings have sharply reduced the levels of asymptomatic DVT in airline passengers, but the effect on symptomatic VTE is unknown, as none of the individuals studied developed symptomatic VTE.

Patient characteristics and predisposing factors for thrombophlebitis nearly mirror those for DVT; thrombophlebitis is a risk factor for the development of DVT, and vice versa.

Lower extremity superficial phlebitis is associated with conditions that increase the risk of thrombosis, including abnormalities of coagulation or fibrinolysis, endothelial dysfunction, infection, venous stasis, intravenous therapy and intravenous drug abuse.

Some 125,000 cases a year have been reported in the United States, but actual incidence of spontaneous thrombophlebitis is unknown.

A fourfold increased incidence from the third to the eight decade in men and a preponderance among women of approximately 55-70%.

The average mean age of affected patients is 60 years.

Thrombophlebitis can develop along the arm, back, or neck veins, the leg is by far the most common site. When it occurs in the leg, the great saphenous vein is usually involved, although other locations are possible.

Thrombosis prevention is initiated with assessing the risk for its development. Some people have a higher risk of developing thrombosis and its possible development into thromboembolism. Some of these risk factors are related to inflammation. "Virchow's triad" has been suggested to describe the three factors necessary for the formation of thrombosis: stasis of blood, vessel wall injury, and altered blood coagulation. Some risk factors predispose for venous thrombosis while others increase the risk of arterial thrombosis.

In people without a detectable thrombophilia, the cumulative risk of developing thrombosis by the age of 60 is about 12%. About 60% of people who are deficient in antithrombin will have experienced thrombosis at least once by age 60, as will about 50% of people with protein C deficiency and about a third of those with protein S deficiency. People with activated protein C resistance (usually resulting from factor V Leiden), in contrast, have a slightly raised absolute risk of thrombosis, with 15% having had at least one thrombotic event by the age of sixty. In general, men are more likely than women to experience repeated episodes of venous thrombosis.

People with factor V Leiden are at a relatively low risk of thrombosis, but may develop thrombosis in the presence of an additional risk factor, such as immobilization. Most people with the prothrombin mutation (G20210A) never develop thrombosis.

The main causes of thrombosis are given in Virchow's triad which lists thrombophilia, endothelial cell injury, and disturbed blood flow.

PTS can affect 23-60% of patients in the two years following DVT of the leg. Of those, 10% may go on to develop severe PTS, involving venous ulcers.

Patients with upper-extremity DVT may develop upper-extremity PTS, but the incidence is lower than that for lower-extremity PTS (15-25%). No treatment or prevention methods are established, but patients with upper-extremity PTS may wear a compression sleeve for persistent symptoms.

Varicose veins are more common in women than in men, and are linked with heredity. Other related factors are pregnancy, obesity, menopause, aging, prolonged standing, leg injury and abdominal straining. Varicose veins are unlikely to be caused by crossing the legs or ankles. Less commonly, but not exceptionally, varicose veins can be due to other causes, as post phlebitic obstruction or incontinence, venous and arteriovenous malformations.

It is often caused by venous reflux. More recent research has shown the importance of pelvic vein reflux (PVR) in the development of varicose veins. Hobbs showed varicose veins in the legs could be due to ovarian vein reflux and Lumley and his team showed recurrent varicose veins could be due to ovarian vein reflux. Whiteley and his team reported that both ovarian and internal iliac vein reflux causes leg varicose veins and that this condition affects 14% of women with varicose veins or 20% of women who have had vaginal delivery and have leg varicose veins. In addition, evidence suggests that failing to look for, and treat pelvic vein reflux can be a cause of recurrent varicose veins.

There is increasing evidence for the role of incompetent perforator veins (or "perforators") in the formation of varicose veins. and recurrent varicose veins.

Varicose veins could also be caused by hyperhomocysteinemia in the body, which can degrade and inhibit the formation of the three main structural components of the artery: collagen, elastin and the proteoglycans. Homocysteine permanently degrades cysteine disulfide bridges and lysine amino acid residues in proteins, gradually affecting function and structure. Simply put, homocysteine is a 'corrosive' of long-living proteins, i.e. collagen or elastin, or lifelong proteins, i.e. fibrillin. These long-term effects are difficult to establish in clinical trials focusing on groups with existing artery decline. Klippel-Trenaunay syndrome and Parkes-Weber syndrome are relevant for differential diagnosis.

Another cause is chronic alcohol consumption due to the vasodilatation side effect in relation to gravity and blood viscosity.

Evidence supports the use of heparin in people following surgery who have a high risk of thrombosis to reduce the risk of DVTs; however, the effect on PEs or overall mortality is not known. In hospitalized non-surgical patients, mortality decreased but not statistically significant. It does not appear however to decrease the rate of symptomatic DVTs. Using both heparin and compression stockings appears better than either one alone in reducing the rate of DVT.

In hospitalized people who have had a stroke and not had surgery, mechanical measures (compression stockings) resulted in skin damage and no clinical improvement. Data on the effectiveness of compression stockings among hospitalized non-surgical patients without stroke is scarce.

The American College of Physicians (ACP) gave three strong recommendations with moderate quality evidence on VTE prevention in non-surgical patients: that hospitalized patients be assessed for their risk of thromboembolism and bleeding before prophylaxis (prevention); that heparin or a related drug is used if potential benefits are thought to outweigh potential harms; and that graduated compression stockings not be used. As an ACP policy implication, the guideline stated a lack of support for any performance measures that incentivize physicians to apply universal prophylaxis without regard to the risks. Goldhaber recommends that people should be assessed at their hospital discharge for persistent high-risk of venous thrombosis, and that people who adopt a heart-healthy lifestyle might lower their risk of venous thrombosis.

In those with cancer who are still walking about yet receiving chemotherapy, LMWH decreases the risk of VTE. Due to potential concerns of bleeding its routine use is not recommended. For people who are having surgery for cancer, it is recommended that they receive anticoagulation therapy (preferably LMWH) in order to prevent a VTE. LMWH is recommended for at least 7–10 days following cancer surgery, and for one month following surgery for people who have a high risk of VTEs.

In adults who have had their lower leg casted or placed in a brace for more than a week, LMWH decreased the risk of VTEs. LMWH is recommended for adults not in hospital with an above-knee cast and a below-knee cast, and is safe for this indication.

Following the completion of warfarin in those with prior VTE, long term aspirin is beneficial.

The overall absolute risk of venous thrombosis per 100,000 woman years in current use of combined oral contraceptives is approximately 60, compared to 30 in non-users. The risk of thromboembolism varies with different types of birth control pills; Compared with combined oral contraceptives containing levonorgestrel (LNG), and with the same dose of estrogen and duration of use, the rate ratio of deep venous thrombosis for combined oral contraceptives with norethisterone is 0.98, with norgestimate 1.19, with desogestrel (DSG) 1.82, with gestodene 1.86, with drospirenone (DRSP) 1.64, and with cyproterone acetate 1.88. Venous thromboembolism occurs in 100–200 per 100,000 pregnant women every year.

Regarding family history, age has substantial effect modification. For individuals with two or more affected siblings, the highest incidence rates is found among those ≥70 years of age (390 per 100,000 in male and 370 per 100,000 in female individuals), whereas the highest incidence ratios compared to those without affected siblings occurred at much younger ages (ratio of 4.3 among male individuals 20 to 29 years of age and 5.5 among female individuals 10 to 19 years of age).

This condition is most common after age 50.

It is more prevalent in females.

There is a hereditary role.

It has been seen in smokers, those who have chronic constipation and in people with occupations which necessitate long periods of standing such as lecturers, nurses, conductors (musical and bus), stage actors, umpires (cricket, javelin, etc.), the Queen's guard, lectern orators, security guards, etc.

Superficial vein thrombosis (SVT) is a type of venous thrombosis, or a blood clot in a vein, which forms in a superficial vein near the surface of the body. Usually there is thrombophlebitis, which is an inflammatory reaction around a thrombosed vein, presenting as a painful induration with erythema. SVT has a limited clinical significance (in terms of morbidity and mortality) when compared to a deep vein thrombosis (DVT), which occurs deeper in the body, at the deep venous system level. If the blood clot is too near from the sapheno-femoral junction there is a bigger risk of pulmonary embolism.

A number of acquired conditions augment the risk of thrombosis. A prominent example is antiphospholipid syndrome, which is caused by antibodies against constituents of the cell membrane, particularly lupus anticoagulant (first found in people with the disease systemic lupus erythematosus but often detected in people without the disease), anti-cardiolipin antibodies, and anti-β-glycoprotein 1 antibodies; it is therefore regarded as an autoimmune disease. In some cases antiphospholipid syndrome can cause arterial as well as venous thrombosis. It is also more strongly associated with miscarriage, and can cause a number of other symptoms (such as livedo reticularis of the skin and migraine).

Heparin-induced thrombocytopenia (HIT) is due to an immune system reaction against the anticoagulant drug heparin (or its derivatives). Though it is named for associated low platelet counts, HIT is strongly associated with risk of venous and arterial thrombosis. Paroxysmal nocturnal hemoglobinuria (PNH) is a rare condition resulting from acquired alterations in the "PIGA" gene, which plays a role in the protection of blood cells from the complement system. PNH increases the risk of venous thrombosis but is also associated with hemolytic anemia (anemia resulting from destruction of red blood cells). Both HIT and PNH require particular treatment.

Hematologic conditions associated with sluggish blood flow can increase risk for thrombosis. For example, sickle-cell disease (caused by mutations of hemoglobin) is regarded as a mild prothrombotic state induced by impaired flow. Similarly, myeloproliferative disorders, in which the bone marrow produces too many blood cells, predispose to thrombosis, particularly in polycythemia vera (excess red blood cells) and essential thrombocytosis (excess platelets). Again, these conditions usually warrant specific treatment when identified.

Cancer, particularly when metastatic (spread to other places in the body), is a recognised risk factor for thrombosis. A number of mechanisms have been proposed, such as activation of the coagulation system by cancer cells or secretion of procoagulant substances. Furthermore, particular cancer treatments (such as the use of central venous catheters for chemotherapy) may increase the risk of thrombosis further.

Nephrotic syndrome, in which protein from the bloodstream is released into the urine due to kidney diseases, can predispose to thrombosis; this is particularly the case in more severe cases (as indicated by blood levels of albumin below 25 g/l) and if the syndrome is caused by the condition membranous nephropathy. Inflammatory bowel disease (ulcerative colitis and Crohn's disease) predispose to thrombosis, particularly when the disease is active. Various mechanisms have been proposed.

Pregnancy is associated with an increased risk of thrombosis. This probably results from a physiological hypercoagulability in pregnancy that protects against postpartum hemorrhage.

The female hormone estrogen, when used in the combined oral contraceptive pill and in perimenopausal hormone replacement therapy, has been associated with a two- to sixfold increased risk of venous thrombosis. The risk depends on the type of hormones used, the dose of estrogen, and the presence of other thrombophilic risk factors. Various mechanisms, such as deficiency of protein S and tissue factor pathway inhibitor, are said to be responsible.

Obesity has long been regarded as a risk factor for venous thrombosis. It more than doubles the risk in numerous studies, particularly in combination with the use of oral contraceptives or in the period after surgery. Various coagulation abnormalities have been described in the obese. Plasminogen activator inhibitor-1, an inhibitor of fibrinolysis, is present in higher levels in people with obesity. Obese people also have larger numbers of circulating microvesicles (fragments of damaged cells) that bear tissue factor. Platelet aggregation may be increased, and there are higher levels of coagulation proteins such as von Willebrand factor, fibrinogen, factor VII and factor VIII. Obesity also increases the risk of recurrence after an initial episode of thrombosis.

A vein disorder is a class of disease involving veins of the circulatory system.

Common vein disorders include:

- Varicose veins

- Deep vein thrombosis

It is known that diabetes causes changes to factors associated with coagulation and clotting, however not much is known of the risk of thromboembolism, or clots, in diabetic patients. There are some studies that show that diabetes increases the risk of thromboembolism; other studies show that diabetes does not increase the risk of thromboembolism. A study conducted in the Umea University Hospital, in Sweden, observed patients that were hospitalized due to an thromboembolism from 1997 to 1999. The researchers had access to patient information including age, sex, vein thromboembolism diagnosis, diagnostic methods, diabetes type and medical history. This study concluded that there is, in fact, an increased risk of thromboembolism development in diabetic patients, possibly due to factors associated with diabetes or diabetes itself. Diabetic patients are twice as likely to develop a thromboembolism than are non-diabetic patient. The exact mechanism of how diabetes increases the risk of clot formation remains unclear and could possibly be a future direction for study.

From previous studies, it is known that long distance air travel is associated with high risk of venous thrombosis. Long periods of inactivity in a limited amount of space may be a reason for the increased risk of blood clot formation. In addition, bent knees compresses the vein behind the knee (the popliteal vein) and the low humidity, low oxygen, high cabin pressure and consumption of alcohol concentrate the blood. A recent study, published in the British Journal of Haematology in 2014, determined which groups of people, are most at risk for developing a clot during or after a long flight. The study focused on 8755 frequent flying employees from international companies and organizations. It found that travelers who have recently undergone a surgical procedure or who have a malignant disease such as cancer or who are pregnant are most at risk. Preventative measures before flying may be taken in these at-risk groups as a solution.

Patients who have undergone kidney transplant have a high risk of developing RVT (about 0.4% to 6%). RVT is known to account for a large proportion of transplanted kidney failures due to technical problems (damage to the renal vein), clotting disorders, diabetes, consumption of ciclosporin or an unknown problem. Patients who have undergone a kidney transplant are commonly prescribed ciclosporin, an immunosuppressant drug which is known to reduce renal blood flow, increase platelet aggregation in the blood and cause damage to the endothelial tissue of the veins. In a clinical study conducted by the Nuffield Department of Surgery at the Oxford Transplant Centre, UK, transplant patients were given low doses of aspirin, which has a some anti-platelet activity. There is risk of bleeding in transplant patients when using anticoagulants like warfarin and herapin. Low dosage of aspirin was used as an alternative. The study concluded that a routine low-dose of aspirin in kidney transplant patients who are also taking ciclosporin significantly reduces the risk of RVT development.

Compression stockings appear to prevent the formation of new ulcers in people with a history of venous ulcers.

The current ‘best’ practice in the UK is to treat the underlying venous reflux once an ulcer has healed. It is questionable as to whether endovenous treatment should be offered before ulcer healing, as current evidence would not support this approach as standard care. EVRA (Early Venous Reflux Ablation) ulcer trial - A UK NIHR HTA funded randomised clinical trial to compare early versus delayed endovenous treatment of superficial venous reflux in patients with chronic venous ulceration opened for recruitment in October 2013. The study hopes to show an increase in healing rates from 60% to 75% at 24 weeks.

Research from the University of Surrey and funded by the Leg Ulcer Charity is currently looking at the psychological impact of having a leg ulcer, on the relatives and friends of the affected person, and the influence of treatment.

The most common cause of chronic venous insufficiency is reflux of the venous valves of superficial veins. This may in turn be caused by several conditions:

- Deep vein thrombosis (DVT), that is, blood clots in the deep veins. Chronic venous insufficiency caused by DVT may be described as postthrombotic syndrome.

- Superficial vein thrombosis.

- Phlebitis

- May–Thurner syndrome. This is a rare condition in which blood clots occur in the iliofemoral vein due to compression of the blood vessels in the leg. The specific problem is compression of the left common iliac vein by the overlying right common iliac artery. Many May-Thurner compressions are overlooked when there is no blood clot. More and more of them get nowadays diagnosed and treated (by stenting) due to advanced imaging techniques.

Deep and superficial vein thrombosis may in turn be caused by thrombophilia, which is an increased propensity of forming blood clots.

Arteriovenous fistula (an abnormal connection or passageway between an artery and a vein) may cause chronic venous insufficiency even with working vein valves.

Chronic venous insufficiency (CVI) is a medical condition in which blood pools in the veins, straining the walls of the vein. The most common cause of CVI is superficial venous reflux which is a treatable condition. As functional venous valves are required to provide for efficient blood return from the lower extremities, this condition typically affects the legs. If the impaired vein function causes significant symptoms, such as swelling and ulcer formation, it is referred to as chronic venous disease. It is sometimes called "chronic peripheral venous insufficiency" and should not be confused with post-thrombotic syndrome in which the deep veins have been damaged by previous deep vein thrombosis.

Most cases of CVI can be improved with treatments to the superficial venous system or stenting the deep system. Varicose veins for example can now be treated by local anesthetic endovenous surgery.

The prevalence of CVI is far higher in women than in men. The Tampere study, which examined the epidemiology of varicose veins in a large cohort of 3284 men and 3590 women, demonstrated that the prevalence of varicose veins in men and women was 18% and 42%, respectively. The condition has been known since ancient times and Hippocrates used bandaging to treat it.

Acquired telangiectasia, not related to other venous abnormalities, for example on the face and trunk, can be caused by factors such as

- Acne rosacea

- Blepharitis

- Environmental damage such as that caused by sun or cold exposure

- Age

- Trauma to skin such as contusions or surgical incisions.

- Radiation exposure such as that experienced during radiotherapy for the treatment of cancer

- Chemotherapy

- Carcinoid syndrome

- Limited systemic sclerosis/scleroderma (a Scleroderma sub-type)

- Chronic treatment with topical corticosteroids may lead to telangiectasia.

- Spider angiomas are a radial array of tiny arterioles that commonly occur in pregnant women and in patients with hepatic cirrhosis and are associated with palmar erythema. In men, they are related to high estrogen levels secondary to liver disease.

- Tempi syndrome

- Smoking

In the past, people used to think that leg varicose veins or telangectasia were caused by high venous pressure or "venous hypertension". However it is now understood that venous reflux disease is usually the cause of these problems (see above for reference for "venous reflux".

Telangiectasia in the legs is often related to the presence of venous reflux within underlying varicose veins. Flow abnormalities within the medium-sized veins of the leg (reticular veins) can also lead to the development of telangiectasia.

Factors that predispose to the development of varicose and telangiectatic leg veins include

- Age: The development of spider veins may occur at any age but usually occurs between 18 and 35 years, and peaks between 50 and 60 years.

- Gender: It used to be thought that females were affected far more than males. However research has shown 79% of adult males and 88% of adult females have leg telangectasia (spider veins).

- Pregnancy: Pregnancy is a key factor contributing to the formation of varicose and spider veins. The most important factor is circulating hormones that weaken vein walls. There's also a significant increase in the blood volume during pregnancy, which tends to distend veins, causing valve dysfunction which leads to blood pooling in the veins. Moreover, later in pregnancy, the enlarged uterus can compress veins, causing higher vein pressure leading to dilated veins. Varicose veins that form during pregnancy may spontaneously improve or even disappear a few months after delivery.

- Lifestyle/occupation: Those who are involved with "prolonged sitting or standing" in their daily activities have an increased risk of developing varicose veins. The weight of the blood continuously pressing against the closed valves causes them to fail, leading to vein distention.

Causes can include pancreatitis, cirrhosis, diverticulitis, and cholangiocarcinoma. It is also a known complication of splenectomy.

In medicine, May-Thurner syndrome (MTS), also known as the iliac vein compression syndrome, is a rare condition in which compression of the common venous outflow tract of the left lower extremity may cause discomfort, swelling, pain or blood clots, called deep venous thrombosis (DVT), in the iliofemoral vein.

The specific problem is compression of the left common iliac vein by the overlying right common iliac artery. This leads to pooling or stasis of blood, predisposing the individual to the formation of blood clots. Uncommon variations of MTS have been described, such as the right common iliac vein getting compressed by the right common iliac artery.

In the 21st century the May-Thurner syndrome definition has been expanded to a broader disease profile known as nonthrombotic iliac vein lesions (NIVL) which can involve both the right and left iliac veins as well as multiple other named venous segments. This syndrome frequently manifests as pain when the limb is dependent (hanging down the edge of a bed/chair) and/or significant swelling of the whole limb.