An embolus that becomes completely stationary when it lodges in a small blood vessel is called a

Anticoagulant drugs are blood thinners. They decrease the blood’s ability to clot, so they can prevent new clots from forming and can stop existing clots from getting bigger. They do not break up or dissolve clots that have already formed. All people with deep venous thrombosis are given anticoagulant drugs.

Doctors usually use low-molecular-weight heparin (such as enoxaparin, dalteparin, or tinzaparin) or fondaparinux given by injection under the skin (subcutaneously), accompanied by warfarin taken by mouth. The injectable drug works immediately, but warfarin takes several days to be fully effective. Once the warfarin has taken effect, people stop taking the injectable drug. For some people (those with cancer or those with recurrent clotting problems despite treatment with anticoagulants by mouth), doctors only use the injectable drug and do not start warfarin.

How long people continue drug treatment (with warfarin or an injectable drug) varies according to the degree of risk. People whose deep vein thrombosis resulted from a specific, temporary cause (such as surgery or a drug they have stopped taking) usually continue drug treatment for 3 to 6 months. When a specific cause is not found, people usually take warfarin for at least 6 months. Warfarin should be continued indefinitely if the cause is not temporary (for example, a blood clotting disorder) or if people have had two or more episodes of deep vein thrombosis.

Use of warfarin increases the risk of bleeding, both internally and externally. To minimize the risk, people taking warfarin must have periodic blood tests to see how much their blood is anticoagulated. Doctors then use the blood test result to adjust the dose of warfarin. The blood tests are usually done once or twice a week for 1 or 2 months, and then every 4 to 6 weeks thereafter.

Direct oral anticoagulants (DOAC) are an alternative to warfarin. Rivaroxaban, apixaban, edoxaban, and dabigatran are DOACs. These drugs have a faster anticoagulant effect than warfarin and are as effective as warfarin for the treatment of blood clots. The effect of DOACs on people's blood is more predictable than the effect of warfarin. Therefore, unlike people taking warfarin, people taking DOACs do not need to have frequent blood tests to adjust the dose. Also, DOACs tend to cause fewer episodes of serious bleeding than warfarin. However, bleeding caused by DOACs can be harder to stop because antidotes for these drugs are not as widely available as antidotes for warfarin.

Excessive bleeding, which may be life-threatening, is the most common complication of anticoagulant drugs. Risk factors for excessive bleeding include being age 65 or older or having

For people who are taking warfarin, doctors can give vitamin K, transfusions of plasma (which contains clotting factors), or prothrombin complex concentrate to reverse the effects of the warfarin and stop the bleeding. For people who are taking heparin, doctors can give protamine to partially reverse the effects.

For people taking some of the DOACs, doctors can give andexanet alfa or prothrombin complex concentrate to reverse the effects of the DOACs and stop the bleeding.

Q. I’m studying for boards and came across a point of confusion. What is the difference between a hemorrhagic and ischemic infarct? I thought that one was due to a thrombus (a stationary clot) and the other was due to an embolus (a clot that forms then moves to another part of the body then gets stuck). But Robbins says that the thrombi usually arise from atherosclerotic plaques in the carotid arteries – but once a chunk breaks off wouldn’t it be an embolus? Also, isn’t hemorrhagic stroke caused by a ruptured vessel like from a brain aneurysm? and ischemic by any type of blood clot? Maybe I’m confused about the two types of strokes or maybe it is the thrombus vs. embolus thing, not really sure. Can you give me some clarification please?

A. First: you’re absolutely right about the definitions of thrombus and embolus. A thrombus is a clot that forms at a particular point in a vessel and stays right there. An embolus is a chunk of something (often a clot – but you can also get fat emboli or bone marrow emboli when you have really severe trauma) that floats downstream and lodges in a smaller vessel.

What is a stroke?
Before we start talking about infarcts, let’s define “stroke.” “Stroke” is a clinical term for symptoms that arise from cerebrovascular problems. The word stroke is usually used in situations where those symptoms come on suddenly and noticeably – like drooping on one side of the face, one-sided paralysis, slurring of speech, or loss of vision on one side. There are three types of cerebrovascular problems: thrombosis, embolism, and hemorrhage. Thrombosis and embolism tend to lead to infarcts (dead tissue) – either ischemic or hemorrhagic in nature. Hemorrhage tends to accumulate in the brain as a mass.

Hemorrhagic vs. ischemic infarcts
Infarcts are divided into two categories based on whether there is hemorrhage present in/around the infarct: hemorrhagic (red) and ischemic (pale) infarcts. Ischemic infarcts are caused by something that cuts off blood supply to a part of the brain – like a thrombus, a big embolus, or even severe vasculitis. They are sometimes called pale infarcts because when you look at them grossly, they look lighter than the surrounding tissue (because of the lack of blood supply). Out of all of the causes of ischemic infarcts, the most common is thrombosis, and the most common places to have thrombosis are: the carotid bifurcation, the origin of the middle cerebral artery, and either end of the basilar artery. Any parts of the brain supplied by these thrombosed arteries would be at risk of ischemia; the extent of ischemia depends a lot on how much collateral flow that part of the brain receives.

Hemorrhagic infarcts are typically associated with embolic events. They are sometimes called red infarcts, because when you look at them grossly, they look red (because of the extravasated blood that’s present). The image above shows a large red infarct at 3 o’clock and a smaller one at 10 o’clock. Wait, didn’t we say emboli could cause ischemic infarcts? Yes – they can. It depends on the size and permanence of the embolus. If you have a big embolus that simply lodges in a vessel and stays put (without dissolving), then you’ll probably get an ischemic infarct. But if you get little emboli that shower an area and then dissolve, or if you have collateral vessels that reperfuse that area of the brain (which contains damaged vessels and tissue, and therefore is more fragile), you’ll probably get a hemorrhagic infarct.

Infarcts due to atherosclerosis
To answer your question about atherosclerosis in the carotid arteries: you could get either a hemorrhagic or an ischemic infarct from that situation. If the the atherosclerotic plaque accumulates and forms a thrombus in the carotid, or if a large chunk of plaque breaks off and lodges in a vessel downstream (and stays put there without dissolving), you’ll get an ischemic infarct. If multiple small chunks break off and shower an area of the brain, especially if they dissolve or if there is strong collateral flow, that could lead to a hemorrhagic infarct.

Can infarcts be caused by ruptured intracranial vessels? 
Finally, you asked about ruptured vessels in the brain. Yes, you can certainly get ruptured intracranial vessels that lead to hemorrhage in in the brain. However, we don’t call that situation a “hemorrhagic infarct,” because the problem is not so much loss of blood flow (infarction) as it is accumulation of blood. It’s kind of a semantic thing; you could get the same symptoms with either infarction or hemorrhage, it’s just that the underlying problem is different, so we name them differently.

Hemorrhage due to rupture of a vessel in the brain can be due to hypertension (which damages vessels and causes them to burst), or rupture of a berry aneurysm, or even trauma. Depending on the size and location of the hemorrhage, a patient might have no symptoms at all, or there might be brain destruction mimicking an infarct, or there might be increased intracranial pressure as blood accumulates in the cranium.

Bottom line
If a patient comes in with symptoms of a stroke, it’s really important for the clinician to figure out the underlying pathology in order to treat the patient safely and effectively.