Embolism

In medicine, an embolism occurs when an object (the embolus, plural emboli) migrates from one part of the body (through circulation) and cause(s) a blockage (occlusion) of a blood vessel in another part of the body. The term was coined in 1848 by Rudolph Carl Virchow.^[1]. This can be contrasted with a "thrombus" which is the formation of a clot within a blood vessel, rather than being carried from somewhere else.

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Classification

There are different types of embolism classified based on the embolic material:

• Thromboembolism - embolism of thrombus or blood clot.
• Fat embolism - embolism of fat droplets.
• Air embolism (also known as a gas embolism) - embolism of air bubbles.
• Septic embolism - embolism of pus containing bacteria.
• Tissue embolism - embolism of small fragments of tissue.
• Foreign body embolism - embolism of foreign materials such as talc and other small objects.
• Amniotic fluid embolism - embolism of amniotic fluid, fetal cells, hair or other debris that enter the mother's blood stream via the placental bed of the uterus and trigger an allergic reaction.

The pathway of the embolus can have 3 different types:

• Anterograde
• Retrograde
• Paradoxical

In anterograde embolism, we say that the movement of emboli is according to the direction of blood flow. However it is otherwise in retreograde embolism, when the weight of the emboli is high enough to oppose the blood flow direction. This is usually only siginificant in blood vessels with low pressure (veins) or emboli of high weight. In paradoxical embolism or also known as crossed embolism, the embolus from veins are crossed to the arterial blood system. This is usually only found in heart defects such as septal defects between the atria or ventricles.

Pathophysiology

In thromboembolism, the thrombus (blood clot) from a blood vessel is completely or partially detached from the site of thrombosis (clot). The blood flow will then carry the embolus (via blood vessels) to various parts of the body where it can block the lumen (vessel cavity) and cause vessel obstruction or occlusion. Note that the free moving thrombus is called an embolus. A thrombus is always attached to the vessel wall and never freely moving in the blood circulation. This is also the key difference for pathologists to determine the cause of a blood clot- by thrombosis or post-mortem blood clot. Vessel obstruction will then lead to different pathological issues such as blood stasis and ischemia.

However not only thromboembolism will cause the obstruction of blood flow in vessels, but any kind of embolism is capable of causing the same problem.

Fat embolism usually occurs when endogenous (from sources within the organism) fat tissue escapes into the blood circulation. The usual cause of fat embolism is therefore the fracture of tubular bones (such as the femur), which will lead to the leakage of fat tissue within the bone marrow into ruptured vessels. Of course there are exogenous (from sources of external origin) causes such as intravenous injection of emulsions.

Air embolism on the other hand is usually always caused by exogenic factors. This can be the rupture of alveoli and inhaled air can be leaked into the blood vessels. Other more common causes include the puncture of subclavian vein by accident or during operation where there is negative pressure. Air is then sucked into the veins by the negative pressure caused by thoracic expansion during inhalation phase of respiration. Air embolism can also happen during intravenous therapy, when air is leaked into the system (however this iatrogenic error in modern medicine is extremely rare).

Gas embolism is usually a common concern for deep sea divers because the gases in our blood (usually nitrogen and helium) can be easily dissolved at higher amount during the descend into deep sea. However when the diver ascends back to the normal atmospheric pressure, gases becomes insoluble causing the formation of small bubbles in blood. This is also known as decompression sickness. This theory is closely related to Henry's Law in physical chemistry.

The other embolisms are rather rare. Septic embolism happens when a purulent tissue (pus containing tissue) is dislodged from its original focus. Tissue embolism is a near equivalent to cancer metastasis which happens when cancer tissue infiltrates blood vessels and small fragments of them are released into the blood stream. Foreign body embolism happens when exogenous (and only exogenous) materials such as talc enters the blood stream and causes occlusion or obstruction of blood circulation. Amniotic fluid embolism is a rare complication of childbirth.

Clinical complications

Assuming a normal circulation, a thrombus or other embolus formed in a systemic vein will always impact in the lungs, after passing through the right side of the heart. This forms a pulmonary embolism that can be a complication of deep-vein thrombosis. Note that, contrary to popular belief, the most common site of origin of pulmonary emboli are the femoral veins, not the deep veins of the calf. Deep veins of the calf are the most common site of thrombi, not emboli origin.

Some congenital abnormalities of the circulation, especially septal defects (holes in the cardiac septum), allow an embolus from a systemic vein to cross into the arterial system and land anywhere in the body (which is known as paradoxical embolism or crossed embolism). The most common such abnormality is patent foramen ovale, occurring in about 25 % of the adult population, but here the defect functions as a valve which is normally closed, because pressure is slightly higher in the left side of the heart. In certain circumstances, e.g. if patient is coughing just when an embolus is passing, passage to the arterial system may occur.

Emboli starting in the heart (from a thrombus in the left atrium secondary to atrial fibrillation or septic emboli from endocarditis) can cause emboli in any part of the body.

An embolus landing in the brain from either the heart or a carotid artery will likely cause an ischemic stroke.

Emboli of cardiac origin are also frequently encountered in clinical practice. Thrombus formation within the atrium in valvular disease occurs mainly in patients with mitral valve disease, and especially in those with mitral valve stenosis with atrial fibrillation (AF). In the absence of AF, pure mitral regurgitation has low incidence of thromboembolism. Absolute risk of emboli in idiopathic AF depends on other risk factors such as increasing 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 to only 5% of inferior ones. Other risk factors include poor ejection fraction (<35%), size of infarct, as well as presence of AF. In the first three months after infarction, left ventricle aneurysms have 10% risk of embolization. Patients with prosthetic valves also carry a significant increase in risk of thromboembolism. Risk varies on the valve type (bioprosthetic or mechanical), the positon (mitral or aortic), and presence of other factors such as AF, left ventricular dysfunction, previous emboli, etc.

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, heart, and lungs.

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