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.

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.

In 2004 the first adequately large scale study on the natural history and long-term prognosis of this condition was reported; this showed that at 16 months follow-up 57.1% of patients had full recovery, 29.5%/2.9%/2.2% had respectively minor/moderate/severe symptoms or impairments, and 8.3% had died. Severe impairment or death were more likely in those aged over 37 years, male, affected by coma, mental status disorder, intracerebral hemorrhage, thrombosis of the deep cerebral venous system, central nervous system infection and cancer. A subsequent systematic review of nineteen studies in 2006 showed that mortality is about 5.6% during hospitalisation and 9.4% in total, while of the survivors 88% make a total or near-total recovery. After several months, two thirds of the cases has resolution ("recanalisation") of the clot. The rate of recurrence was low (2.8%).

In children with CVST the risk of death is high. Poor outcome is more likely if a child with CVST develops seizures or has evidence of venous infarction on imaging.

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

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).

Cerebral venous sinus thrombosis is rare, with an estimated 3-4 cases per million annual incidence in adults. While it may occur in all age groups, it is most common in the third decade. 75% are female. Given that older studies show no difference in incidence between men and women, it has been suggested that the use of oral contraceptives in women is behind the disparity between the sexes. A 1995 report from Saudi Arabia found a doubled incidence at 7 cases per 100,000; this was attributed to the fact that Behçet's disease, which increases risk of CVST, is more common in the Middle East.

A 1973 report found that CVST could be found on autopsy (examination of the body after death) in nine percent of all people. Many of these were elderly and had neurological symptoms in the period leading up to their death, and many suffered from concomitant heart failure.

In children, a Canadian study reported in 2001 that CVST occurs in 6.7 per million annually. 43% occur in the newborn (less than one month old), and a further 10% in the first year of life. Of the newborn, 84% were already ill, mostly from complications after childbirth and dehydration.

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 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.

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.

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.

The most common types of congenital thrombophilia are those that arise as a result of overactivity of coagulation factors. They are relatively mild, and are therefore classified as "type II" defects. The most common ones are factor V Leiden (a mutation in the "F5" gene at position 1691) and prothrombin G20210A, a mutation in prothrombin (at position 20210 in the 3' untranslated region of the gene).

The rare forms of congenital thrombophilia are typically caused by a deficiency of natural anticoagulants. They are classified as "type I" and are more severe in their propensity to cause thrombosis. The main ones are antithrombin III deficiency, protein C deficiency and protein S deficiency. Milder rare congenital thrombophilias are factor XIII mutation and familial dysfibrinogenemia (an abnormal fibrinogen). It is unclear whether congenital disorders of fibrinolysis (the system that destroys clots) are major contributors to thrombosis risk. Congenital deficiency of plasminogen, for instance, mainly causes eye symptoms and sometimes problems in other organs, but the link with thrombosis has been more uncertain.

Blood group determines thrombosis risk to a significant extent. Those with blood groups other than type O are at a two- to fourfold relative risk. O blood group is associated with reduced levels of von Willebrand factor – because of increased clearance – and factor VIII, which is related to thrombotic risk .

Thrombophlebitis causes include disorders related to increased tendency for blood clotting and reduced speed of blood in the veins such as prolonged immobility; prolonged traveling (sitting) may promote a blood clot leading to thrombophlebitis but this occurs relatively less. High estrogen states such as pregnancy, estrogen replacement therapy, or oral contraceptives are associated with an increased risk of thrombophlebitis.

Specific disorders associated with thrombophlebitis include superficial thrombophlebitis which affects veins near the skin surface, deep venous thrombosis which affects deeper veins, and pulmonary embolism. Those with familial clotting disorders such as protein S deficiency, protein C deficiency, or factor V Leiden are also at increased risk of thrombophlebitis. Thrombophlebitis can be found in people with vasculitis including Behçet's disease. Thrombophlebitis migrans can be a sign of malignancy - Trousseau sign of malignancy..

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.

Hypercoagulability in pregnancy, particularly due to inheritable thrombophilia, can lead to placental vascular thrombosis. This can in turn lead to complications like early-onset hypertensive disorders of pregnancy, pre-eclampsia and small for gestational age infants (SGA). Among other causes of hypercoagulability, Antiphospholipid syndrome has been associated with adverse pregnancy outcomes including recurrent miscarriage. Deep vein thrombosis has an incidence of one in 1,000 to 2,000 pregnancies in the United States, and is the second most common cause of maternal death in developed countries after bleeding.

Currently laboratory testing is not as reliable as observation when it comes to defining the parameters of Thrombotic Storm. Careful evaluation of possible thrombosis in other organ systems is pertinent in expediting treatment to prevent fatality.Preliminary diagnosis consists of evidence documented with proper imaging studies such as CT scan, MRI, or echocardiography, which demonstrate a thromboembolic occlusion in the veins and/or arteries. Vascular occlusions mentioned must include at least two of the clinic events:

- Deep venous thrombosis affecting one (or more) limbs and/or pulmonary embolism.

- Cerebral vein thrombosis.

- Portal vein thrombosis, hepatic vein, or other intra-abdominal thrombotic events.

- Jugular vein thrombosis in the absence of ipsilateral arm vein thrombosis and in the absence of ipsilateral central venous access.

- Peripheral arterial occlusions, in the absence of underlying atherosclerotic vascular disease,

- resulting in extremity ischemia and/or infarction.

- Myocardial infarction, in the absence of severe coronary artery disease

- Stroke and/or transient ischemic attack, in the absence of severe atherosclerotic disease and at an age less than 60 years.

- Central retinal vein and/or central retinal arterial thrombosis.

- Small vessel thrombosis affecting one or more organs, systems, or tissue; must be documented by histopathology.

In addition to the previously noted vascular occlusions, development of different thromboembolic manifestations simultaneously or within one or two weeks must occur and the patient must have an underlying inherited or acquired hypercoagulable state (other than Antiphospholipid syndrome)

Vascular occlusion is a blockage of a blood vessel, usually with a clot. It differs from thrombosis in that it can be used to describe any form of blockage, not just one formed by a clot. When it occurs in a major vein, it can, in some cases, cause deep vein thrombosis. The condition is also relatively common in the retina, and can cause partial or total loss of vision. An occlusion can often be diagnosed using Doppler sonography (a form of ultrasound).

Some medical procedures, such as embolisation, involve occluding a blood vessel to treat a particular condition. This can be to reduce pressure on aneurysms (weakened blood vessels) or to restrict a haemorrhage. It can also be used to reduce blood supply to tumours or growths in the body, and therefore restrict their development. Occlusion can be carried out using a ligature; by implanting small coils which stimulate the formation of clots; or, particularly in the case of cerebral aneurysms, by clipping.

Superficial vein thrombosis extension to the deep vein system and/or recurrence of SVT.

Suppurative thrombophlebitis is suspected when erythema extends significantly beyond the margin of the vein and is likely to be associated with significant fever. If suspected, antibiotic treatment, surgical drainage and potentially vein excision are indicated.

Venous thromboembolism can occur with superficial vein thrombosis. Estimates of the percentage of patients with SVT who also have DVT vary between 6% and 53%, and symptomatic pulmonary embolism has been reported in 0% to 10% of patients with SVT.

Blood clots are a relatively common occurrence in the general population and are seen in approximately 1-2% of the population by age 60. Typically blood clots develop in the deep veins of the lower extremities, deep vein thrombosis (DVT) or as a blood clot in the lung, pulmonary embolism (PE). A very small number of people who develop blood clots have a more serious and often life-threatening condition, known as Thrombotic Storm (TS). TS is characterized by the development of more than one blood clot in a short period of time. These clots often occur in multiple and sometimes unusual locations in the body and are often difficult to treat. TS may be associated with an existing condition or situation that predisposes a person to blood clots such as injury, infection, or pregnancy. In many cases a risk assessment will identify interventions that will prevent the formation of blood clots.

While the mechanism or pathogenesis is not completely understood mostly due to its rarity, the medical community has developed a new interest in learning more about this syndrome. Dr. Craig S. Kitchens first described TS in six case studies. In these cases he described a collection of similar features observed in six patients, suggesting this may be accounted for by a new syndrome.

Unfractionated heparin, low molecular weight heparin, warfarin (not to be used during pregnancy) and aspirin remain the basis of antithrombotic treatment and prophylaxis both before and during pregnancy.

While the consensus among physicians is the safety of the mother supersedes the safety of the developing fetus, changes in the anticoagulation regimen during pregnancy can be performed to minimize the risks to the developing fetus while maintaining therapeutic levels of anticoagulants in the mother.

The main issue with anticoagulation in pregnancy is that warfarin, the most commonly used anticoagulant in chronic administration, is known to have teratogenic effects on the fetus if administered in early pregnancy. Still, there seems to be no teratogenic effect of warfarin before six weeks of gestation. However, unfractionated heparin and low molecular weight heparin do not cross the placenta.

The following factors increase the risk of developing PTS:

- age > 65

- proximal DVT

- a second DVT in same leg as first DVT (recurrent ipsilateral DVT)

- persistent DVT symptoms 1 month after DVT diagnosis

- obesity

- poor quality of anticoagulation control (i.e. dose too low) during the first 3 months of treatment

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.

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.

Nontraumatic intraparenchymal hemorrhage most commonly results from hypertensive damage to blood vessel walls e.g.:

- hypertension

- eclampsia

- drug abuse,

but it also may be due to autoregulatory dysfunction with excessive cerebral blood flow e.g.:

- reperfusion injury

- hemorrhagic transformation

- cold exposure

- rupture of an aneurysm or arteriovenous malformation (AVM)

- arteriopathy (e.g. cerebral amyloid angiopathy, moyamoya)

- altered hemostasis (e.g. thrombolysis, anticoagulation, bleeding diathesis)

- hemorrhagic necrosis (e.g. tumor, infection)

- venous outflow obstruction (e.g. cerebral venous sinus thrombosis).

Nonpenetrating and penetrating cranial trauma can also be common causes of intracerebral hemorrhage.

It can be diagnosed by histomorphologic examination of the placenta and is characterized by fetal vessel thrombosis and clustered fibrotic chorionic villi without blood vessels.

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.