what should i expect? aneurysm-cerebral artery?

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I just found out that my mum has an aneurysm in
her left cerebral artery,
all i know is it's
about 5mm, they have done a lumbar puncher,
waiting for the results. they have sent her home
and want to do a coiling over the next two weeks.
She is 49 average health.

Just wanting to know what could be ahead.
thanks
Endovascular coiling is an increasingly popular treatment option, as it has a high success rate, with 77% of people making a significant improvement or a full recovery. This procedure is also less invasive compared to conventional clipping and recovery times are usually quicker.
That is from a UK hospital.

From a US site...and this is where you come in...
At home:
You may be advised not to participate in any strenuous activities. Your physician will instruct you about when you can return to work and resume normal activities.
Notify your physician to report any of the following:
* fever and/or chills
* increased pain, redness, swelling, or bleeding or other drainage from the insertion site
* coolness, numbness and/or tingling, or other changes in the affected extremity
* any changes in bodily functions or neurological changes, such as extreme headache, seizure, or loss of consciousness

...so you will have to stop your mum playing football for a bit!
There is a link to the US site which describes eveything in detail if you want to know, but don't you and your mum be scared. If nothing is done it could rupture and that is an emergency.
Look after her and I wish you both all the luck in the world.

six66 if you read this I am sorry for what happened.  (+ info)

Right posterior communicating artery aneurysm, anterior communicating artery aneurysm right otitis externa.?

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Patient was admitted with suspicion of intracranial aneurysm. On the following day, that patient underwent a three-vessel cerebral angiogram that demonstrated a posterior communicating artery aneurysm and questionable anterior communicating artery aneurysm. The patient underwent a right craniotomy for clipping of the right posterior communicating artery aneurysm and anterior communicating artery aneurism. Postoperatively, the patient was observed in the surgical care unit until his mental status was stabilized. The palsy and ptosis noted preoperatively resolved during the post surgical course. The patient has been moving without assistance and tolerating food well. The patient was also seen by the ENT service during the hospitalization for his otitis external and their recommendations were as follows. How would you code both the principal diagnosis and any other diagnoses that arise from this case ?
Principal:
437.3 Cerebral aneurysm, nonruptured

Others:
01.24 Other craniotomy
39.52 Other repair of aneurysm
89.6 Circulatory monitoring
380.22 Other acute otitis externa
89.06 Consultation, described as limited  (+ info)

If a patient was diagnoses with right posterior communicating artery aneurysm; anterior communicating artery?

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communicating artery aneurysm; right otitis externa what is the final diagnosies and the principal diagnosis and medical code for this and the procedure code
Oh man, I knew it would come to this, medical students or doctors using Y/A! to practice medicine. What next, Supreme Court Justices asking about the Commerce Clause?  (+ info)

IS RIGHT VENTRICULR INFARCTION = POSTERIOR WALL INFARCTION?

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  (+ info)

How can an aneurysm lead to a blood clot which would cause an infarction???

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A patient suffers from severe leg pain while golfing. And pees discolored urine. He was misdiagnosed with muscle trauma when in reality he had a blocked artery in his leg caused by a popliteal artery aneurysm. By the time the blockage was diagnosed, a great deal of muscle tissue had already died and the patient eventually gets an infarction. My question is, how does a Popliteal Artery Aneurysm lead to a blood clot???
Haha, I know exactly where you're getting this from!! House, right?? (sorry, I just LOVE that show)

Anyways, blood clotting is a big risk with aneurysms. Clots can break off and travel through the bloodstream until they get stuck. Normally, treatment is given quickly, and amputation or invasive measures like that are not required. But if it is not diagnosed soon enough, muscle tissue dies, and the limb may have to be amputated.

If you want a more in-depth explanation, here's a good article: http://www.evtoday.com/AAA/2003%20Files/Popliteal%20Artery%20Aneurysms.html  (+ info)

What is the risk of a less than 2mm cerebral aneurysm?

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I had an MRA and they found a tiny saccular aneurysm measuring less than 2mm maximum diameter directed posteriorly at the origin of left A1 segment of anterior cerebral artery. I am 29 years old. Any general information about aneurysms and the danger of the location would be greatly appreciated.
http://www.healthatoz.com/healthatoz/Atoz/common/standard/transform.jsp?requestURI=/healthatoz/Atoz/ency/cerebral_aneurysm.jsp

Looks like there is a 1% chance each year that it could rupture. Maybe that's similar to the sum of other risks of great bodily injury like driving, going into a convenience store or going to a pizzaria in NY.

But you should find out what kinds of activities might be more dangerous and make sure your blood pressure stays good! Since,you've been to a doctor, you have probaly heard this by now.

Good luck.  (+ info)

Do you know of Cerebral Vascular Accident (CVA) and Middle Cerebral Artery (MCA)?

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What is Cerebral Vascular Accident (CVA)?
What is Middle Cerebral Artery (MCA)?
Is CVA and MCA is related?
How do they connected?
It is all about Nursing process assignment...
Need to know all about it in Nursing ways....
Please explain details with website or any references....
I need this information to do my case study of Nursing course...
Very important one....
Doctor diagnosis this patient with...
1. Left MCA infarct
2. Hypertension emergency with organ damage retinohemorragic
3. Uncontrolled DM secondary to not complaint to meds
Help please....
A CVA is an artery in the brain which has grow. The surroundings of this cel became thinner. The risk is that the braincell can collapse. It's a very vital organ and normally the damage is that braincells and arteries can be damaged. This can paralyze parts of the body. When there's a CVA on the left side it's possible you cannot speak: Afasie.
It's important the patient has enough rest. The revalidationperiod can take 6-12 months. It's important to exercise every day.  (+ info)

What will a partial obstruction in a coronary artery likely cause?

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a. pulmonary embolus
b. hypertension
c. angina attack
d. myocardial infarction
c.

Can we do all of your homework for you?  (+ info)

How will I know if the artery begins to close again?

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I've had a myocardial infarction on whom PTCA+STENT was done 2 1/2 years back.
To understand your question you must understand what a myocardial infarction is.

This term refers to the death of a certain segment of the heart muscle (myocardium), usually the result of a focal complete blockage in one of the main coronary arteries or a branch thereof.

The main cause of myocardial infarction is atherosclerosis in the coronary arteries. This event results in impaired contractility of the heart muscle within seconds, and is initially restricted to the affected segment.

The myocardial ischemia or infarction begins in the endocardium (the inner lining of the heart) and spreads to the epicardium (the outer lining of the heart). Irreversible heart damage will occur if the blockage is complete for at least 15-20 minutes. Irreversible damage occurs maximally in the area at risk, and when the occlusion is maintained for 4-6 hours. Most of the damage occurs in the first 2-3 hours. Restoration of flow within the first 4-5 hours is associated with salvage of the heart muscle, but the salvage is greater if flow is restored in the first 1-2 hours. A major determinant of death and illness is the size of the infarct. Increasing the oxygen supply to the involved site of blockage by coronary reperfusio is more effective in salvaging the myocardium than decreasing oxygen demand.

The onset of acute Q-wave myocardial infarction occurs commonly in the morning hours shortly after arising, when there is increasing adrenergic activity, as well as increased blood fibrinogen levels and increased platelet (blood cell) adhesiveness. Non Q wave infarction does not show this circadian rhythm.

The traditional concept that myocardial infarctions can be classified as transmural or nontransmural on the basis of the presence or absence of Q waves is misleading, since autopsy studies have demonstrated convincingly that pathologic Q waves may be associated with nontransmural infarction and may be absent with transmural infarction. These misnomers have been replaced by the terms Q-wave infarction and nonQ-wave infarction for transmural and nontransmural infarction, respectively.

The evolution of a non-Q-wave infarction is charcterized by a lack of development of an abnormal Q wave and by the appearance of reversible ST-T-wave changes with ST depression that usually returns to normal over a few days, but occasionally is permanent. Differentiation between these two types of infarctions has become entrenched, since there are major differences in their pathogenesis, clinical manifestations, treatment, and prognosis. The initiating events in the pathogenesis of Q-wave and non-Q-wave infarction are thought to be identical, namely, coronary occlusion induced by thrombus superimposed on a plaque together with vasoconstriction.

There is considerable evidence, however, to indicate that in non-Q-wave infarction, early spontaneus reperfusion occurs, the mechanism of which remains uncertain. In contrast, in Q-wave infarction, the coronary occlusion is sustained at least for a long enough period to result in extensive necrosis.
One explanation for early spontaneous reperfusion is the lack of sustained vasoconstriction, which may contribute to ocusion. The evidence supporting the existence of early spontaneous reperfusion in non-Q-wave infarction is as follows:

1. Coronary angiographic studies performed in the early hours after onset show that only 20-30% of patients have complete coronary occlusion of the infarct-related vessels;but for Q-wave infarction it is about 80 to 90%.


2. Infarct size is routinely much less than observed with Q wave infarction, which is consistent with salvage by early reperfusion.

3. Peak plasma CK levels are reached on an average of 12 to 13 h after onset of symptoms, indicating early washout of the enzyme, as opposed to about 27 h after Q-wave infarction.

4. Reperfusion-induced contraction necrosis is extremely common, as it is in patients who undergo early reperfusion induced by thrombolytic therapy.

5. Acute mortality rates are around 2 to 3 percent, compared with 10 percent for Q-wave infarction.

6. The complications are minimal compared with those after a Q-wave infarction.

7. Finally, the long-term prognosis is characterized by recurrent episodes of reinfarction, so that after about 2 years, survival is the same as that after Q-wave infarction.

Quite often with the initial heart attack over half of the patients have significant obstructive atherosclerosis in only one vessel. However, in a recent study two fifths of the patients with acute myocardial infarction had angiographic evidence of multiple complex coronary plaques, which were associated with a less favorable in-hospital course. The presence of these plaques with complex morphologic features is the angiographic hallmark of unstable coronary syndromes and correlates with pathologic plaque and thrombus

I'm not a Doctor... I'm just a Corpsman...  (+ info)

Do you know the data sheet for examination of a patient of carotid artery stenosis?

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This is a part of vascular surgery.
Carotid artery stenosis may lead to cerebral stroke.
Carotid artery stenosis is when plaque forms in the carotid arteries, constricting the flow of blood to the brain. The carotid arteries are the main arteries coming from your heart to your head. The risk is that, if there is plaque, a small piece could break off and get lodged in a smaller vessel in your brain, causing lack of blood to that part of the brain. This can result in in a TIA, or mini stroke, or can even result in something as serious as a brain bleed. An ultrasound is the simplest and safest method for determining plaque, as well as velocity of the blood flow. Velocity at any point of stenosis is a key factor. I could go on about what range velocities should be in, but that opens up a whole worksheet of math problems that I can't begin to explain here.

It would be best to consult your physician if I did not answer your question here, especially as I am not sure what you mean by data sheet. If you are wanting the math equations for velocity, you can e-mail me and I will send you something.  (+ info)

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