Embolism

Embolism
Classification and external resources
ICD-10 I74., I82., O88., T79.0-T79.1
ICD-9 444.9
DiseasesDB 18165
MeSH D004617

In medicine, an embolism (plural embolisms) occurs when an object (the embolus, plural emboli) migrates from one part of the body (through circulation) and causes 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 is in contrast with a thrombus, or clot, which forms at the blockage point within a blood vessel and is not carried from somewhere else.

Contents

Classification

There are different types of emboli.

Material

They can be classified based on the embolic material:

Pathway

The pathway of the embolus can be one of three types:

In anterograde embolism, the movement of emboli is in the direction of blood flow. In retrograde embolism, however, the emboli move in opposition to the blood flow direction; this is usually significant only in blood vessels with low pressure (veins) or with emboli of high weight. In paradoxical embolism, also known as crossed embolism, an embolus from the veins crosses to the arterial blood system. This is generally found only with heart problems 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.[2] A thrombus is always attached to the vessel wall and is never freely moving in the blood circulation. This is also the key difference for pathologists to determine the cause of a blood clot, either by thrombosis or by 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 also 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. There are also exogenous (from sources of external origin) causes such as intravenous injection of emulsions.

An 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 the 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 the 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 a common concern for deep-sea divers because the gases in our blood (usually nitrogen and helium) can be easily dissolved at higher amounts during the descent into deep sea. However, when the diver ascends to the normal atmospheric pressure, the gases become insoluble, causing the formation of small bubbles in the blood. This is also known as decompression sickness or the Bends. This phenomenon is explained by 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 enter the blood stream and cause 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 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 embolization. Patients with prosthetic valves also carry a significant increase in risk of thromboembolism. Risk varies, based on the valve type (bioprosthetic or mechanical); the positon (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, heart, and lungs.

References

  1. Hellemans, Alexander; Bryan Bunch (1988). The Timetables of Science. New York, New York: Simon and Schuster. pp. 317. ISBN 0671621300. 
  2. Howland, Richard D.; Mycek, Mary J., Pharmacology, Lippincott’s illustrated reviews (3rd ed. ed.), Philadelphia : Lippincott Williams & Wilkins, c2006., p. 227, ISBN 0781741181