Preventing the development of blood clots in the upper extremities is done by accessing the risk of the development of such clots.The traditional treatment for thrombosis is the same as for a lower extremity DVT, and involves systemic anticoagulation to prevent a pulmonary embolus. Some have also recommended thrombolysis with catheter directed alteplase. If there is thoracic outlet syndrome or other anatomical cause then surgery can be considered to correct the underlying defect.

Management of the underlying defect is proportional to the severity of the clinical presentation. Leg swelling and pain is best evaluated by vascular specialists (vascular surgeons, interventional cardiologists, interventional radiologists) who both diagnose and treat arterial and venous diseases to ensure that the cause of the extremity pain is evaluated. The diagnosis needs to be confirmed with some sort of imaging that may include magnetic resonance venography, venogram and usually confirmed with intravascular ultrasound because the flattened vein may not be noticed on conventional venography. In order to prevent prolonged swelling or pain from the consequences of the backed up blood from the compressed iliac vein, flow needs to be improved out of the leg. Uncomplicated cases may be managed with compression stockings.

Severe May-Thurner syndrome may require thrombolysis if there is a recent onset of thrombosis, followed by angioplasty and stenting of the iliac vein after confirming the diagnosis with a venogram or an intravascular ultrasound. A stent may be used to support the area from further compression following angioplasty. As the name implies, there classically is not a thrombotic component in these cases, but thrombosis may occur at any time.

If the patient has extensive thrombosis, it may be appropriate to consider pharmacologic and/or mechanical (also known as pharmacomechanical) thrombectomy. This is currently being studied to determine whether this will decrease the incidence of post-thrombotic syndrome.

TIF is a rare condition with a .7% frequency, and an mortality rate approaching 100% without surgical intervention. Immediate diagnosis and intervention of an TIF is critical for the surgical intervention success. 25-30% of TIF patients who reach the operating room survive. Recently, the incidence of TIF may have declined due to advances in tracheostomy tube technology and the introduction of the bedside percutaneous dilatational tracheostomy (PDT).

May-Thurner syndrome (MTS) is thought to represent between two and five percent of lower-extremity venous disorders. May-Thurner syndrome is often unrecognized; however, current estimates are that this condition is three times more common in women than in men. The classic syndrome typically presents in the second to fourth decades of life. In the 21st century in a broader disease profile, the syndrome acts as a permissive lesion and becomes symptomatic when something else happens such as, following trauma, a change in functional status such as swelling following orthopaedic joint replacement.

It is important to consider May-Thurner syndrome in patients who have no other obvious reason for hypercoagulability and who present with left lower extremity thrombosis. To rule out other causes for hypercoagulation, it may be appropriate to check the antithrombin, protein C, protein S, factor V Leiden, and prothrombin G20210A.

Venography will demonstrate the classical syndrome when causing deep venous thrombosis.

May-Thurner syndrome in the broader disease profile known as nonthrombotic iliac vein lesions (NIVLs) exists in the symptomatic ambulatory patient and these lesions are usually not seen by venography. Morphologically, intravascular ultrasound (IVUS) has emerged as the best current tool in the broader sense. Functional testing such as duplex ultrasound, venous and interstitial pressure measurement and plethysmography may sometimes be beneficial. Compression of the left common iliac vein may be seen on pelvic CT.

The condition is relatively rare. It usually presents in young and otherwise healthy patients, and also occurs more often in males than females. The syndrome also became known as "effort-induced thrombosis" in the 1960s, as it has been reported to occur after vigorous activity, though it can also occur due to anatomic abnormality such as clavicle impingement or spontaneously. It may develop as a sequela of thoracic outlet syndrome. It is differentiated from secondary causes of upper extremity caused by intravascular catheters. Paget–Schroetter syndrome was described once for a viola player who suddenly increased practice time 10-fold, creating enough repetitive pressure against the brachiocephalic and external jugular veins to cause thrombosis.

Symptoms may include sudden onset of pain, warmth, redness, blueness and swelling in the arm. Diagnosis is usually confirmed with an ultrasound. These DVTs have the potential to cause a pulmonary embolism.

Epidemiological data is elusive owing to the wide variety of clinical presentation. In the U.S., incidence is estimated to be at 5–10 cases per 100,000 per year. Minor compression of the inferior vena cava during pregnancy is a relatively common occurrence. It is seen most prevalently when women lie on their back or right side. 90% of women lying in the supine position during pregnancy experience inferior vena cava syndrome; however, not all of the women display symptoms.

There are many causes of TOS. The most frequent cause is trauma, either sudden (as in a clavicle fracture caused by a car accident), or repetitive (as in a legal secretary who works with his/her hands, wrists, and arms at a fast paced desk station with non-ergonomic posture for many years). TOS is also found in certain occupations involving lots of lifting of the arms and repetitive use of the wrists and arms.

One cause of arterial compression is trauma, and a recent case involving fracture of the clavicle has been reported.

The two groups of people most likely to develop TOS are those suffering from neck injuries due to traffic accidents and those who use computers in non-ergonomic postures for extended periods of time. TOS is frequently a repetitive stress injury (RSI) caused by certain types of work environments. Other groups which may develop TOS are athletes who frequently raise their arms above the head (such as swimmers, volleyball players, dancers, badminton players, baseball pitchers, and weightlifters), rock climbers, electricians who work long hours with their hands above their heads, and some musicians.

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.

TOS can be attributed to one or more of the following factors:

- Congenital abnormalities are frequently found in persons with TOS. These include cervical rib, prolonged transverse process, and muscular abnormalities (e.g., in the scalenus anterior muscle, a sickle-shaped scalenus medius) or fibrous connective tissue anomalies.

- Trauma (e.g., whiplash injuries) or repetitive strain is frequently implicated.

- Rarer acquired causes include tumors, hyperostosis, and osteomyelitis

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.

History and examination by a physician with characteristic signs and symptoms are sufficient in many cases in ruling out systemic causes of venous hypertension such as hypervolemia and heart failure. An ultrasound (usually a lower limbs venous ultrasonography) can detect venous obstruction or valvular incompetence as the cause, and is used for planning venous ablation procedures, but it is not necessary in suspected venous insufficiency where surgical intervention is not indicated.

Venous stasis, or venostasis, is a condition of slow blood flow in the veins, usually of the legs. Venous stasis is a risk factor for forming blood clots in veins (venous thrombosis), as with the deep veins of the legs (deep vein thrombosis or DVT). Causes of venous stasis include long periods of immobility that can be encountered from driving, flying, bed rest/hospitalization, or having an orthopedic cast. Recommendations by clinicians to reduce venous stasis and DVT/PE often encourage increasing walking, calf exercises, and intermittent pneumatic compression when possible.

Prevention is possible with Thrombosis prophylaxis methods and practices.

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.

The innominate artery usually crosses the trachea at the ninth cartilage ring, however this can vary from the sixth to the thirteenth cartilage ring in patients. A TIF runs between the trachea and the innominate artery. Through this connection blood from within the artery may pass into the trachea or alternatively air from within the trachea may cross into the artery.

TIF is a late complication of a tracheotomy and is associated with prolonged endotracheal intubation, as a result of cuff over inflation or a poorly positioned tracheostomy tube. Over inflation of the cuff causes the tracheostomy tube to erode into the posterior aspect of the innominate artery leading to the formation of a fistula. The pathogenesis of an TIF by the aforementioned method is pressure necrosis by tracheostomy tube on the tracheal wall. An TIF can also occur due to innominate artery injury as a result of an bronchoscopy.

Patients whose tracheotomies are placed beneath the third tracheal ring cartilage and patients with innominate arteries crossing higher on the trachea have an increased risk of developing an TIF. Other factors contributing to the development of TIF include steroids, which weaken the endotracheal mucosa, episodes of hypotension in which the pressure in the tracheostomy tube exceeds that of the endotracheal mucosa, and radiation therapy.

An endotracheal tumor can mimic a TIF and present with massive bleeding during a rigid bronchoscopy.

The radiocephalic arteriovenous fistula (RC-AVF) is a shortcut between cephalic vein and radial artery at the wrist. It is the recommended first choice for hemodialysis access. Possible underlying causes for failure are stenosis and thrombosis especially in diabetics and those with low blood flow such as due to narrow vessels, arteriosclerosis and advanced age. Reported patency of fistulae after 1 year is about 62.5%.

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.

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.

This condition is usually asymptomatic. The aberrant artery usually arises just distal to the left subclavian artery and crosses in the posterior part of the mediastinum on its way to the right upper extremity. In 80% of individuals it crosses behind the esophagus. Such course of this aberrant vessel may cause a vascular ring around the trachea and esophagus.

Dysphagia due to an aberrant right subclavian artery is termed dysphagia lusoria, although this is a rare complication. In addition to dysphagia, aberrant right subclavian artery may cause stridor, dyspnoea, chest pain, or fever. An aberrant right subclavian artery may compress the recurrent laryngeal nerve causing a palsy of that nerve, which is termed Ortner's syndrome.

The aberrant right subclavian artery frequently arises from a dilated segment of the proximal descending aorta, the so-called Diverticulum of Kommerell (which was named for the German Radiologist, Burkhard Friedrich Kommerell (1901–1990), who discovered it in 1936). It is alternatively known as a lusorian artery.

Thrombophlebitis occurs almost equally between women and men, though males do have a slightly higher possibility. The average age of developing thrombophlebitis, based on analyzed incidents, is 54 for men and 58 for women.

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.

The three factors of Virchow's triad—venous stasis, hypercoagulability, and changes in the endothelial blood vessel lining (such as physical damage or endothelial activation)—contribute to DVT and are used to explain its formation. Other related causes include activation of immune system components, the state of microparticles in the blood, the concentration of oxygen, and possible platelet activation. Various risk factors contribute to DVT, though many at high risk never develop it.

Acquired risk factors include the strong risk factor of older age, which alters blood composition to favor clotting. Other important acquired risk factors include major surgery and trauma, both of which may increase the risk because of tissue factor from outside the vascular system entering the blood. In orthopedic surgery, venous stasis may be temporarily provoked by a cessation of blood flow as part of the procedure. Cancer can grow in and around veins, causing venous stasis, and can also stimulate increased levels of tissue factor. Pregnancy causes blood to favor clotting, and in the postpartum, placental tearing releases substances that favor clotting. Oral contraceptives and hormonal replacement therapy increase the risk through a variety of mechanisms, including altered blood coagulation protein levels and reduced fibrinolysis.

The disease term venous thromboembolism (VTE) includes the development of either DVT or pulmonary embolism (PE). Genetic factors that increase the risk of VTE include deficiencies of three proteins that normally prevent blood from clotting—protein C, protein S, and antithrombin—in addition to non-O blood type and mutations in the factor V and prothrombin genes. Deficiencies in antithrombin, protein C, and protein S are rare but strong, or moderately strong, risk factors. These three thrombophilia increase the risk of VTE by about 10 times. Factor V Leiden, which makes factor V resistant to inactivation by activated protein C, and the genetic variant prothrombin G20210A, which causes increased prothrombin levels, are predominantly expressed in Caucasians. They moderately increase risk for VTE, by three to eight times for factor V Leiden and two to three times for prothrombin G20210A. Having a non-O blood type roughly doubles VTE risk. Non-O blood type is common in all races, making it an important risk factor. Individuals without O blood type have higher blood levels of von Willebrand factor and factor VIII than those with O blood type, increasing the likelihood of clotting.

Some risk factors influence the location of DVT within the body. In isolated distal DVT, the profile of risk factors appears distinct from proximal DVT. Transient factors, such as surgery and immobilization, appear to dominate, whereas thrombophilias and age do not seem to increase risk. In upper-extremity DVT, the most important risk factor is having a central venous catheter, and thoracic outlet syndrome also increases risk.

DVA can be diagnosed through the Cerebral venous sinus thrombosis with collateral drainage. DVA can also be found diagnosed with Sturge–Weber syndrome and can be found through leptomeningeal angiomatosis. Demyelinating disease has also been found to enlarge Medulla veins.

Aberrant subclavian artery, or aberrant subclavian artery syndrome, is a rare anatomical variant of the origin of the right or left subclavian artery. This abnormality is the most common congenital vascular anomaly of the aortic arch, occurring in approximately 1% of individuals.

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

Common vein disorders include:

- Varicose veins

- Deep vein thrombosis

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).