It is an obstruction caused by an embolus, a piece of material that causes a blockage within a blood vessel.
The embolus can be a blood clot (thrombus), a fat globule (fat embolism), an air bubble or other gas (air embolism), or foreign material.
An embolism can cause a partial or complete blockage of blood flow in the affected vessel. This obstruction (a vascular occlusion) can affect a part of the body distant from the origin of the embolus.
An embolism in which the embolus is a piece of thrombus is called a thromboembolism. An embolism is usually a pathological event, an accompanying illness or injury.
Sometimes, it is created intentionally for a therapeutic reason, such as stopping bleeding or killing a cancerous tumor by cutting off its blood supply. This therapy is called embolization.
There are different types of stroke, some of which are listed below.
Embolism can be classified based on where it enters circulation, either in the arteries or veins. Arterial embolisms follow, and if they do not dissolve along the way, they lodge in a more distal part of the systemic circulation.
Sometimes multiple classifications apply; for example, a pulmonary embolism is also classified as an arterial embolism, in the sense that the clot follows the pulmonary artery that carries deoxygenated blood out of the heart.
However, pulmonary embolism is generally classified as a form of venous embolism because the embolus forms in the veins, for example, deep vein thrombosis.
Pulmonary embolism is also sometimes classified as an arterial embolism because the clot follows the pulmonary artery that carries deoxygenated blood away from the heart.
However, pulmonary embolism is generally classified as venous embolism, because the embolus forms in the veins.
Arterial embolism can cause occlusion in any part of the body. It is a leading cause of heart attack and tissue death due to obstruction of the blood supply.
An embolus that lodges in the brain either from the heart or from a carotid artery will most likely cause a stroke due to ischemia.
Arterial embolism is the leading cause of infarction (which can also be caused by arterial compression, rupture, or pathological vasoconstriction).
An arterial embolus may originate in the heart (from a thrombus in the left atrium after atrial fibrillation or a septic embolus resulting from endocarditis ). Emboli of cardiac origin are common in clinical practice.
Thrombus formation within the atrium occurs mainly in patients with mitral valve disease, especially those with stenosis (narrowing) of the mitral valve, with atrial fibrillation (AF).
Signs and symptoms of an arterial embolism
In the absence of atrial fibrillation, pure mitral regurgitation has a low incidence of thromboembolism.
For example, symptoms of myocardial infarction mainly include chest pain, dyspnea, sweating (an excessive form of sweating), weakness, dizziness, nausea, vomiting, and palpitations.
Symptoms of limb infarction include coldness, decreased or absent pulse beyond the site of obstruction, pain, muscle spasm, numbness and tingling, paleness, and muscle weakness, possibly to the degree of paralysis in the affected limb.
Commonly occluded sites
Arterial emboli often occur in the legs and feet. Some can happen in the brain, causing a stroke, or in the heart, causing a heart attack.
Risk factors for thromboembolism, the leading cause of arterial embolism, include impaired blood flow (as in atrial fibrillation and mitral stenosis), injury or damage to an arterial wall, and hypercoagulability (such as an increase in platelet count ).
The risk of emboli formation in atrial fibrillation depends on other risk factors such as age, hypertension, diabetes, recent heart failure, or previous stroke.
Thrombus formation can also occur within the ventricles, occurring in approximately 30% of anterior wall myocardial infarctions, compared to only 5% of inferior ones.
Other risk factors are poor ejection fraction (<35%), infarct size, and the presence of atrial fibrillation. In the first three months after infarction, left ventricular aneurysms to have a 10% risk of emboli formation.
Patients with prosthetic valves also have a significantly increased risk of thromboembolism.
The risk varies depending on the type of valve (bioprosthetic or mechanical), the position (mitral or aortic), and the presence of other factors such as atrial fibrillation, left ventricular dysfunction, and anterior emboli.
Emboli often have more severe consequences in the so-called “end circulation” – areas of the body that do not have a redundant blood supply, such as the brain and heart.
Endocarditis increases the risk of thromboembolism due to a mixture of the factors mentioned above.
Atherosclerosis in the aorta and other large blood vessels is a common risk factor for thromboembolism and cholesterol embolism. The legs and feet are the primary impact sites for these guys.
Therefore, risk factors for atherosclerosis are also risk factors for arterial embolization:
- Old age.
- Cigarette smoking
- Hypertension (high blood pressure)
- Hyperlipidemia, e.g., hypercholesterolemia, hypertriglyceridemia, elevated lipoprotein A or apolipoprotein B, and decreased levels of high-density lipoprotein cholesterol.
- Mellitus diabetes.
- Sedentary lifestyle.
Other important risk factors for arterial embolism include:
- Recent surgery (for both thromboembolism and air embolism).
- Previous stroke or cardiovascular disease.
- History of long-term intravenous therapy (for air embolism).
The clot can then move into an artery and cause arterial embolization.
Assuming average circulation, an embolus formed in a systemic vein will always impact the lungs after passing through the right side of the heart.
This will form a pulmonary embolism causing a blockage of the primary lung artery and can be a complication of deep vein thrombosis.
The most common sites of origin for pulmonary emboli are the femoral veins. The deep veins of the calf are the most common sites for current thrombi.
It is a blockage of an artery in the lungs by a substance that has moved from another part of the body through the bloodstream (embolism). Pulmonary embolism usually results from a blood clot in the leg that travels to the lung.
The risk of blood clots increases with cancer, prolonged bed rest, smoking, stroke, certain genetic conditions, estrogen-based medications, pregnancy, obesity, and after some types of surgery.
A small proportion of cases are due to embolization of air, fat, or amniotic fluid. The diagnosis is based on the signs and symptoms combined with the test results. A blood test known as a D-dimer will rule out the condition if the risk is low.
Otherwise, a CT pulmonary angiogram, pulmonary ventilation/perfusion scan, or ultrasound of the legs can confirm the diagnosis. Deep vein thrombosis and pulmonary embolism are known as venous thromboembolism (VTE).
Efforts to prevent pulmonary embolism include starting to move as soon as possible after surgery, exercises for the lower legs during periods of sitting, and the use of blood thinners after some types of surgery.
Treatment for a pulmonary embolism
Treatment is typical with blood thinners such as heparin or warfarin. They are often recommended for six months or more.
Severe cases may require thrombolysis with medications such as tissue plasminogen activator (Tpa) or may require surgery such as a pulmonary thrombectomy. If anticoagulants are not appropriate, a vena cava filter can be used.
Pulmonary emboli affect about 430,000 people each year in Europe. In the United States, between 300,000 and 600,000 cases occur each year, resulting in between 50,000 and 200,000 deaths. The rates are similar for men and women. They become more common as people get older.
Signs and symptoms of a pulmonary embolism
A pulmonary embolism can include shortness of breath, chest pain, particularly when inhaling, and coughing up blood.
Symptoms of a blood clot in the leg may also be present, such as a red, hot, swollen, and painful leg.
Signs of a pulmonary embolism include low oxygen levels in the blood, rapid breathing, a rapid heart rate, and sometimes a mild fever. Severe cases can lead to fainting, abnormally low blood pressure, and sudden death.
Symptoms of pulmonary embolism are typically sudden and may include one or many of the following: dyspnea (shortness of breath), tachypnea (rapid breathing), chest pain of a ‘pleuritic’ nature (made worse by breathing), cough and hemoptysis (coughing up blood).
More severe cases can include signs such as cyanosis (blue discoloration, usually of the lips and fingers), collapse, and circulatory instability due to decreased blood flow through the lungs and to the left side of the heart.
Approximately 15% of all cases of sudden death are attributable to a pulmonary embolism.
Physical exam for a pulmonary embolism
On physical examination, the lungs are generally normal. Occasionally, a pleural rub may be audible over the affected area of the lung (mainly in a pulmonary embolism with a heart attack).
Sometimes a pleural effusion is exudative, detectable by decreased percussion notes, audible breath sounds, and vocal resonance.
Right ventricular enlargement can be detected as an elevation of the left parasternal gland, a solid pulmonary component of the second heart sound, or an increase in jugular venous pressure.
A low fever may occur, particularly if associated with bleeding or pulmonary infarction.
Because smaller pulmonary emboli tend to lodge in more peripheral areas without collateral circulation, they are more likely to cause pulmonary infarction and small effusions (both painful) but not hypoxia, dyspnea, or hemodynamic instability such as tachycardia.
More extensive pulmonary embolisms, which tend to lodge centrally, typically cause dyspnea, hypoxia, low blood pressure, rapid heart rate, and fainting but are often painless because there is no pulmonary infarction due to collateral circulation.
The classic presentation for pulmonary embolism with pleuritic pain, dyspnea, and tachycardia is probably caused by a sizeable fragmented embolism causing large and small pulmonary embolisms.
Therefore, small pulmonary embolisms are often overlooked because they cause pleuritic pain alone without any other findings.
And large pulmonary embolisms are often overlooked because they are painless and mimic other conditions that often cause electrocardiogram changes and slight increases in levels of troponin and brain-type natriuretic peptides.
Pulmonary embolisms are sometimes described as massive, submassive, and nonmassive, depending on clinical signs and symptoms.
Although the exact definitions of these are not clear, an accepted definition of massive pulmonary embolism is one in which there is hemodynamic instability such as sustained low blood pressure, slow heart rate, or no pulse.
Approximately 90% of emboli stem from proximal deep vein thrombosis of the leg or pelvic venous thrombosis (DVT). Deep vein thromboses run the risk of displacement and migration into the pulmonary circulation.
The conditions are generally thought of as a continuum called venous thromboembolism (VTE).
The development of thrombosis is classically due to a group of causes called Virchow’s triad (alterations in blood flow, factors in the wall of the vessels, and factors that affect the properties of the blood). Often there is more than one risk factor present.
Causes of a pulmonary embolism
Alterations in blood flow: immobilization (after surgery, long-distance flight), injury, pregnancy, obesity, and cancer (procoagulant).
Vascular wall factors: surgery, catheterization causing direct injury (“endothelial injury”).
Paradoxical (venous to arterial): In paradoxical embolism, also known as cross embolism, an embolus from the veins pass into the arterial blood system.
This is usually found only with heart problems such as septal defects (holes in the heart’s septum) between the atria or ventricles.
The most common abnormality is a persistent foramen ovale, which occurs in approximately 25% of the adult population, but here the defect functions as a valve that is usually closed because the pressure is slightly higher on the left side of the heart.
Sometimes, for example, if a patient coughs just as an embolus is passing, it can cross into the arterial system.
The direction of the plunger can be of two types:
In antegrade embolism, the movement of the emboli is in the direction of blood flow. In retrograde embolism, however, the emboli move in opposition to the law of blood flow; this is usually significant only in low-pressure blood vessels (veins) or with high-weight emboli.
The word embolism comes from the Greek ἐμβολισμός, which means “interposition.”
Prevention and treatment of thrombosis
Thrombosis prevention, also known as thrombosis prophylaxis, are treatments to prevent blood clots from forming within a blood vessel.
Some people are at higher risk for blood clots than others. Preventive measures or interventions are usually started after surgery, as people are at higher risk of immobility.
There are medication-based interventions and non-medication-based interventions. The risk of developing blood clots can be modified by lifestyle modifications, discontinuing oral contraceptives, and weight loss.
In high-risk people, both interventions are often used. Treatments to prevent blood clots are balanced against the risk of bleeding.
One of the goals of blood clot prevention is to limit venous stasis as it is a significant risk factor for the formation of blood clots in the deep veins of the legs.
Venous stasis can occur during long periods of immobility. Thrombosis prevention is also recommended during air travel.
Thrombosis prophylaxis effectively prevents the formation of blood clots, their lodging in the veins, and their development into thromboembolism that can travel through the circulatory system to cause obstruction and subsequent tissue death in other organs.
Clarence Crafoord is credited with the first use of thrombosis prophylaxis in the 1930s.
The development of blood clots can be interrupted and prevented by using medications, changes in risk factors, and other interventions.
Some risk factors can be modified. These would be weight loss, increased exercise, and cessation of oral contraceptives. Moving during travel periods is a modifiable behavior.
Prevention of blood clots includes medications that interrupt the complex clotting cascade and change the proteins necessary for clotting. Antiplatelet drugs also have an effect in preventing clot formation.
Treatment will differ significantly from clot prevention if a blood clot has already formed in a blood vessel. Hemolytic drugs are used. These are medications that will help dissolve the clot.
Physical interventions are contraindicated due to the risk of the clot migrating to distant sites such as the heart, brain, and lungs. Once a clot has formed, the person will be prescribed bed rest and remain relatively immobile until the lump is undetectable.
Thrombosis prophylaxis is often prescribed for hospitalized patients on a routine basis. Blood thinners are often prescribed. Preoperatively, some patients receive low molecular weight heparin once daily.
Additional risk factors such as obesity, illness, malignancies, lengthy surgeries, and immobility can influence the prescribed dose.
Anticoagulant medications prevent blood clots from forming in people at high risk of developing them. Treatment of blood clots that have already started is controlled with anti-hemolytic (‘anticoagulants’).
The following list describes some of the most common medications to prevent blood clots.
Since blood clotting is inhibited, a side effect is typically bleeding. However, it can be reversed by giving a drug that stops the bleeding or discontinuing the medication itself.
Administration of anticoagulants is often given before the start of the operation. There are concerns about the potential for an increased risk of bleeding, and many surgeons begin anticoagulants within the first 6 hours after surgery.
An international registry and risk assessment calculator is being used to centralize data on postoperative venous thrombosis and its prevention. Hospitals are implementing a multidisciplinary approach to preventing blood clots.
This includes proper risk assessment, monitoring missed doses of medication, and establishing a ‘patient-centered’ approach endorsed by the Joint Commission.
Recommendations regarding blood clot prevention vary widely among physicians and treatment centers.
Investigations continue to clarify these discrepancies. Tests are being developed for the metabolic status of hypercoagulability (tendency to form blood clots).