Jugular vein thrombosis is a condition that may occur due to infection, intravenous drug use or malignancy. Jugular vein thrombosis can have a varying list of complications, including: systemic sepsis, pulmonary embolism, and papilledema. Though characterized by a sharp pain at the site of the vein, it can prove difficult to diagnose, because it can occur at random.

Cavernous sinus thrombosis is a specialised form of cerebral venous sinus thrombosis, where there is thrombosis of the cavernous sinus of the basal skull dura, due to the retrograde spread of infection and endothelial damage from the danger triangle of the face. The facial veins in this area anastomose with the superior and inferior ophthalmic veins of the orbit, which drain directly posteriorly into the cavernous sinus through the superior orbital fissure. Staphyloccoal or Streptococcal infections of the face, for example nasal or upper lip pustules may thus spread directly into the cavernous sinus, causing stroke-like symptoms of double vision, squint, as well as spread of infection to cause meningitis.

A venous thrombus is a blood clot (thrombus) that forms within a vein. "Thrombosis" is a term for a blood clot occurring inside a blood vessel. A common type of venous thrombosis is a deep vein thrombosis (DVT), which is a blood clot in the deep veins of the leg. If the thrombus breaks off (embolizes) and flows towards the lungs, it can become a pulmonary embolism (PE), a blood clot in the lungs.

An inflammatory reaction is usually present, mainly in the superficial veins and, for this reason this pathology is called most of the time thrombophlebitis. The inflammatory reaction and the white blood cells play a role in the resolution of venous clots.

The initial treatment for venous thromboembolism is typically with either low molecular weight heparin (LMWH) or unfractionated heparin. LMWH appears to have lower rates of side effects; however, both result in similar rates of survival.

Superficial venous thromboses cause discomfort but generally not serious consequences, as do the deep venous thromboses (DVTs) that form in the deep veins of the legs or in the pelvic veins. Nevertheless, they can progress to the deep veins through the perforator veins or, they can be responsible for a lung embolism mainly if the head of the clot is poorly attached to the vein wall and is situated near the sapheno-femoral junction.

When a blood clot breaks loose and travels in the blood, this is called a venous thromboembolism (VTE). The abbreviation DVT/PE refers to a VTE where a deep vein thrombosis (DVT) has moved to the lungs (PE or pulmonary embolism).

Since the veins return blood to the heart, if a piece of a blood clot formed in a vein breaks off it can be transported to the right side of the heart, and from there into the lungs. A piece of thrombus that is transported in this way is an "embolus": the process of forming a thrombus that becomes embolic is called a "thromboembolism". An embolism that lodges in the lungs is a "pulmonary embolism" (PE). A pulmonary embolism is a very serious condition that can be fatal depending on the dimensions of the embolus. Venous thromboembolism (VTE) refers to both DVTs and PEs.

Systemic embolisms of venous origin can occur in patients with an atrial or ventricular septal defect, through which an embolus may pass into the arterial system. Such an event is termed a paradoxical embolism.

Common signs and symptoms of DVT include pain or tenderness, swelling, warmth, redness or discoloration, and distention of surface veins, although about half of those with the condition have no symptoms. Signs and symptoms alone are not sufficiently sensitive or specific to make a diagnosis, but when considered in conjunction with known risk factors, can help determine the likelihood of DVT. In most suspected cases, DVT is ruled out after evaluation, and symptoms are more often due to other causes, such as cellulitis, Baker's cyst, musculoskeletal injury, or lymphedema. Other differential diagnoses include hematoma, tumors, venous or arterial aneurysms, and connective tissue disorders.

Phlegmasia cerulea dolens is a very large and dangerous type of DVT. It is characterized by an acute and almost total venous occlusion of the entire extremity outflow, including the iliac and femoral veins. The leg is usually painful, tinged blue in color, and swollen, which may result in venous gangrene.

Symptoms may begin quickly or slowly depending on the size of the embolus and how much it blocks the blood flow. Symptoms of embolisation in an organ vary with the organ involved but commonly include:

- Pain in the involved body part

- Temporarily decreased organ function

Later symptoms are closely related to infarction of the affected tissue. This may cause permanently decreased organ function.

For example, symptoms of myocardial infarction mainly include chest pain, dyspnea, diaphoresis (an excessive form of sweating), weakness, light-headedness, nausea, vomiting, and palpitations.

Symptoms of limb infarction include coldness, decreased or no pulse beyond the site of blockage, pain, muscle spasm, numbness and tingling, pallor and muscle weakness, possibly to the grade of paralysis in the affected limb.

In those with suspected DVT, a clinical assessment of probability can be useful to determine which tests to perform. The most studied clinical prediction rule is the Wells score.

Wells score or criteria: (possible score −2 to 9)

1. Active cancer (treatment within last 6 months or palliative): +1 point

2. Calf swelling ≥ 3 cm compared to asymptomatic calf (measured 10 cm below tibial tuberosity): +1 point

3. Swollen unilateral superficial veins (non-varicose, in symptomatic leg): +1 point

4. Unilateral pitting edema (in symptomatic leg): +1 point

5. Previous documented DVT: +1 point

6. Swelling of entire leg: +1 point

7. Localized tenderness along the deep venous system: +1 point

8. Paralysis, paresis, or recent cast immobilization of lower extremities: +1 point

9. Recently bedridden ≥ 3 days, or major surgery requiring regional or general anesthetic in the past 12 weeks: +1 point

10. Alternative diagnosis at least as likely: −2 points

Those with Wells scores of two or more have a 28% chance of having DVT, those with a lower score have 6% odds. Alternatively, Wells scores can be categorized as high if greater than two, moderate if one or two, and low if less than one, with likelihoods of 53%, 17%, and 5%, respectively.

Arterial emboli often occur in the legs and feet. Some may occur in the brain, causing a stroke, or in the heart, causing a heart attack. Less common sites include the kidneys, intestines, and eyes.

Embolism can be classified as to where it enters the circulation either in arteries or in veins. Arterial embolism are those that follow and, if not dissolved on the way, lodge in a more distal part of the systemic circulation. Sometimes, multiple classifications apply; for instance a pulmonary embolism is classified as an arterial embolism as well, in the sense that the clot follows the pulmonary artery carrying deoxygenated blood away from the heart. However, pulmonary embolism is generally classified as a form of venous embolism, because the embolus forms in veins, e.g. deep vein thrombosis.

Arterial embolism can cause occlusion in any part of the body. It is a major cause of infarction, tissue death due to the blockage of blood supply.

An embolus lodging in the brain from either the heart or a carotid artery will most likely be the cause of a stroke due to ischemia.

An arterial embolus might originate in the heart (from a thrombus in the left atrium, following atrial fibrillation or be a septic embolus resulting from endocarditis). Emboli of cardiac origin are frequently encountered in clinical practice. Thrombus formation within the atrium occurs mainly in patients with mitral valve disease, and especially in those with mitral valve stenosis (narrowing), with atrial fibrillation (AF). In the absence of AF, pure mitral regurgitation has a low incidence of thromboembolism.

The risk of emboli forming in AF depends on other risk factors such as age, hypertension, diabetes, recent heart failure, or previous stroke.

Thrombus formation can also take place within the ventricles, and it occurs in approximately 30% of anterior-wall myocardial infarctions, compared with only 5% of inferior ones. Some other risk factors are poor ejection fraction (<35%), size of infarct, and the presence of AF. In the first three months after infarction, left-ventricle aneurysms have a 10% risk of emboli forming.

Patients with prosthetic valves also carry a significant increase in risk of thromboembolism. Risk varies, based on the valve type (bioprosthetic or mechanical); the position (mitral or aortic); and the presence of other factors such as AF, left-ventricular dysfunction, and previous emboli.

Emboli often have more serious consequences when they occur in the so-called "end circulation": areas of the body that have no redundant blood supply, such as the brain and heart.

Nine in ten people with sinus thrombosis have a headache; this tends to worsen over the period of several days, but may also develop suddenly (thunderclap headache). The headache may be the only symptom of cerebral venous sinus thrombosis. Many patients have symptoms of stroke: inability to move one or more limbs, weakness on one side of the face or difficulty speaking. This does not necessarily affect one side of the body as in the more common "arterial" stroke.

40% of people have seizures, although it is more common in women who develop sinus thrombosis peripartum (in the period before and after giving birth). These are mostly seizures affecting only one part of the body and unilateral (occurring on one side), but occasionally the seizures are generalised and rarely they lead to status epilepticus (persistent or recurrent seizure activity for a long period of time).

In the elderly, many of the aforementioned symptoms may not occur. Common symptoms in the elderly with this condition are otherwise unexplained changes in mental status and a depressed level of consciousness.

The pressure around the brain may rise, causing papilledema (swelling of the optic disc) which may be experienced as visual obscurations. In severely raised intracranial pressure, the level of consciousness is decreased, the blood pressure rises, the heart rate falls and the patient assumes an abnormal posture.

The most common conditions associated with thrombophilia are deep vein thrombosis (DVT) and pulmonary embolism (PE), which are referred to collectively as venous thromboembolism (VTE). DVT usually occurs in the legs, and is characterized by pain, swelling and redness of the limb. It may lead to long-term swelling and heaviness due to damage to valves in the veins. The clot may also break off and migrate (embolize) to arteries in the lungs. Depending on the size and the location of the clot, this may lead to sudden-onset shortness of breath, chest pain, palpitations and may be complicated by collapse, shock and cardiac arrest.

Venous thrombosis may also occur in more unusual places: in the veins of the brain, liver (portal vein thrombosis and hepatic vein thrombosis), mesenteric vein, kidney (renal vein thrombosis) and the veins of the arms. Whether thrombophilia also increases the risk of arterial thrombosis (which is the underlying cause of heart attacks and strokes) is less well established.

Thrombophilia has been linked to recurrent miscarriage, and possibly various complications of pregnancy such as intrauterine growth restriction, stillbirth, severe pre-eclampsia and abruptio placentae.

Protein C deficiency may cause purpura fulminans, a severe clotting disorder in the newborn that leads to both tissue death and bleeding into the skin and other organs. The condition has also been described in adults. Protein C and protein S deficiency have also been associated with an increased risk of skin necrosis on commencing anticoagulant treatment with warfarin or related drugs.

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)

Thrombotic Storm has been seen in individuals of all ages and races. The initial symptoms of TS present in a similar fashion to the symptoms experienced in deep vein thrombosis. Symptoms of a DVT may include pain, swelling and discoloration of the skin in the affected area. As with DVTs patients with TS may subsequently develop pulmonary emboli. Although the presentation of TS and DVTs are similar, TS typically progresses rapidly, with numerous clots occurring within a short period of time. After the formation of the initial clot a patient with TS typically begins a “clotting storm” with the development of multiple clots throughout the body. Rapid progression within a short period of time is often seen, affecting multiple organs systems. The location of the clot is often unusual or found in a spot in the body that is uncommon such as the dural sinus. Patients tend to respond very well to anticoagulation such as coumadin or low molecular weight heparin but may become symptomatic when treatment is withheld.

While the key clinical characteristics of thrombotic storm are still being investigated, it is believed that the clinical course is triggered by a preexisting condition, known as a hypercoagulable state. These can include such things as pregnancy, trauma or surgery. Hypercoagulable states can be an inherited or acquired risk factor that then serves as a trigger to initiate clot formation. However, in a subset of patient with TS a trigger cannot be identified. Typically people with TS will have no personal or family history of coagulations disorders.

The following symptoms or signs are often associated with thrombophlebitis, although thrombophlebitis is not restricted to the veins of the legs.

In terms of complications, one of the most serious occurs when the superficial blood clot is associated with a deeper venous thrombosis; this can then dislodge, traveling through the heart and occluding the dense capillary network of the lungs This is a pulmonary embolism which can be life-threatening to the affected individual.

Cerebral venous sinus thrombosis (CVST) is the presence of acute thrombosis (a blood clot) in the dural venous sinuses, which drain blood from the brain. Symptoms may include headache, abnormal vision, any of the symptoms of stroke such as weakness of the face and limbs on one side of the body, and seizures. The diagnosis is usually by computed tomography (CT/CAT scan) or magnetic resonance imaging (MRI) employing radiocontrast to demonstrate obstruction of the venous sinuses by thrombus.

Treatment is with anticoagulants (medication that suppresses blood clotting), and rarely thrombolysis (enzymatic destruction of the blood clot). Given that there is usually an underlying cause for the disease, tests may be performed to look for these. The disease may be complicated by raised intracranial pressure, which may warrant surgical intervention such as the placement of a shunt.

Thrombophilia can be congenital or acquired. "Congenital thrombophilia" refers to inborn conditions (and usually hereditary, in which case ""hereditary thrombophilia"" may be used) that increase the tendency to develop thrombosis, while, on the other hand, "acquired thrombophilia" refers to conditions that arise later in life.

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 paradoxical embolism, also called a crossed embolism, refers to an embolus which is carried from the venous side of circulation to the arterial side, or vice versa. It is a kind of stroke or other form of arterial thrombosis caused by embolism of a thrombus (blood clot), air, tumor, fat, or amniotic fluid of venous origin, which travels to the arterial side through a lateral opening in the heart, such as a patent foramen ovale, or arteriovenous shunts in the lungs.

The opening is typically an atrial septal defect, but can also be a ventricular septal defect.

Paradoxical embolisms represent two percent of arterial emboli.

Findings of tenderness, induration, pain and/or erythema along the course of a superficial vein usually establish a clinical diagnosis, especially in patients with known risk factors. In addition, there is often a palpable, sometimes nodular cord, due to thrombus within the affected vein. Persistence of this cord when the extremity is raised suggests the presence of thrombus.

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.

Passage of a clot (thrombus) from a systemic vein to a systemic artery. When clots in systemic veins break off (embolize), they travel first to the right side of the heart and, normally, then to the lungs where they lodge, causing pulmonary embolism. On the other hand, when there is a hole at the septum, either upper chambers of the heart (an atrial septal defect) or lower chambers of the heart (ventricular septal defects), a clot can cross from the right to the left side of the heart, then pass into the systemic arteries as a paradoxical embolism. Once in the arterial circulation, a clot can travel to the brain, block a vessel there, and cause a stroke (cerebrovascular accident).

Post-thrombotic syndrome (PTS), also called postphlebitic syndrome and venous stress disorder is a medical condition that may occur as a long-term complication of deep vein thrombosis (DVT).

Signs and symptoms of PTS in the leg may include:

- pain (aching or cramping)

- heaviness

- itching or tingling

- swelling (edema)

- varicose veins

- brownish or reddish skin discoloration

- ulcer

These signs and symptoms may vary among patients and over time. With PTS, these symptoms typically are worse after walking or standing for long periods of time and improve with resting or elevating the leg.

PTS lowers a person's quality of life after DVT, specifically with regards to physical and psychological symptoms and limitations in daily activities.