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|Classification and external resources|
|ICD-10||I74, I82, O88, T79.0-T79.1|
In medicine, an embolism is the lodging of an embolus, which may be a blood clot, a fat globule or a gas bubble, in the bloodstream. This can cause a blockage in a blood vessel. Such a blockage (vascular occlusion) may affect a part of the body distanced from the actual site of the embolism. This is in contrast to a thrombus, which causes a blockage at the site of origin.
The word embolism comes from the Greek ἐμβολισμός, meaning "interposition".
There are different types of embolism, some of which are listed below.
Arterial or venous
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.
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 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 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.
Assuming a normal circulation, an embolus formed in a systemic vein will always impact in the lungs, after passing through the right side of the heart. This will form a pulmonary embolism that will result in a blockage of the main artery of the lung and can be a complication of deep-vein thrombosis. The most common sites of origin of pulmonary emboli are the femoral veins. The deep veins of the calf are the most common sites of actual thrombi.
Paradoxical (venous to arterial)
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 (holes in the cardiac septum) between the atria or ventricles. 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. Sometimes, for example if a patient coughs just when an embolus is passing, it might cross to the arterial system.
The direction of the embolus can be one of two 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.
- Britannica concise encyclopedia 2007
- MedlinePlus > Arterial embolism Sean O. Stitham, MD and David C. Dugdale III, MD. Also reviewed by David Zieve, MD. Reviewed last on: 5/8/2008. Alternative link: 
- MR of Fat Embolism Brain Injury from Fat Embolism