STEMI + cerebral hemorrhage

[ohyeahbaby]

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In short, old dude presents with STEMI, they give him streptokinase, and a few hours later the dude is comatose with asymmetric pupils and irregular breathing. The answer to that question was that he had an MI and that the treatment caused a cerebral hemorrhage.

Okay, that's cool - but where is the blood coming out of? for example, you have a tube with blood in it, and after you injected the streptokinase or tPA, you now have a tube with thinner blood in it, but blood is coming out now. So is there a hole in the tube now?

let's say someone presents with a stroke - you don't administer a thrombolytic until you get your CT scan because yes, even though it's most likely a clot, it could still be an aneurysm (i.e. the hole in the tube). If you administer the thrombolytic without knowing it was an aneurysm, then the pt will essentially bleed to death. That, I get. There is a hole in the tube. Thin blood will rush out of it. But if there is no hole in the tube, then it doesn't matter how thin the blood is because there's no hole to come out of, right?

I am definitely missing something, and would appreciate any clarification. It's something that's always bothered me. Like when they tell you that someone presents with a nose that won't stop bleeding because he took too much blood thinner. I get why the blood would rush out of his nose (i.e. it's thinner), but I don't get what it's rushing through.

thank you!

 

[Phloston]

In short, old dude presents with STEMI, they give him streptokinase, and a few hours later the dude is comatose with asymmetric pupils and irregular breathing. The answer to that question was that he had an MI and that the treatment caused a cerebral hemorrhage.

Okay, that's cool - but where is the blood coming out of? for example, you have a tube with blood in it, and after you injected the streptokinase or tPA, you now have a tube with thinner blood in it, but blood is coming out now. So is there a hole in the tube now?

let's say someone presents with a stroke - you don't administer a thrombolytic until you get your CT scan because yes, even though it's most likely a clot, it could still be an aneurysm (i.e. the hole in the tube). If you administer the thrombolytic without knowing it was an aneurysm, then the pt will essentially bleed to death. That, I get. There is a hole in the tube. Thin blood will rush out of it. But if there is no hole in the tube, then it doesn't matter how thin the blood is because there's no hole to come out of, right?

I am definitely missing something, and would appreciate any clarification. It's something that's always bothered me. Like when they tell you that someone presents with a nose that won't stop bleeding because he took too much blood thinner. I get why the blood would rush out of his nose (i.e. it's thinner), but I don't get what it's rushing through.

thank you!

Interesting question.

In the absence of a stroke, if the guy has had an MI, it's likely that he may have also had concomitant Hx of long-standing hypertension, which means he may have had multiple Charcot-Bouchard and/or a saccular aneurysm(s). Exacerbation of the former with thrombolytics could lead to respiratory difficulties due to basal ganglia intraparenchymal haemorrhage; the latter could further compress the posterior cerebral artery or CNIII if rupture does not occur, whereas haemorrhage in this case would have led to severe headache, but not necessarily a comatose state.

With a comatose state and pupillary asymmetry, I'd actually think Charcot-Bouchard aneurysmal rupture; with pupillary asymmetry, I'd think comorbid CNIII compression secondary to an exasperated posterior communicating artery saccular aneurysm, although the CB aneurysm alone is more likely.

 

[ohyeahbaby]

phloston, I may have misunderstood you - so you're basically saying that "thick" blood didn't exacerbate the aneurysm, but "thin" blood did? I can't seem to wrap my mind around this. If anything, i'd think that thicker blood would be more likely to complicate things than thin blood would. The fact that the blood is thick or thin - assuming there was no rupture, how does that make the endothelium weaker and more prone to being stretched out enough so that it would cause problems in its immediate surroundings?

Also, how does that explain the nose bleed (or GI bleed, etc...) that some people get when they overdose on a strong thrombolytic?

 

[AndyRSC]

http://www.medscape.com/viewarticle/463997_3
About halfway down.

 

[StIGMA]

I am definitely missing something, and would appreciate any clarification. It's something that's always bothered me. Like when they tell you that someone presents with a nose that won't stop bleeding because he took too much blood thinner. I get why the blood would rush out of his nose (i.e. it's thinner), but I don't get what it's rushing through.

thank you!

Any small vessel at any given time in your body is prone to a small tear/bleed due to high pressure or stress or weak architecture or infection or remodelling or whatever, and they are normally repaired efficiently so you never notice. If you are on an anticoagulant, these tiny tears are not able to be repaired efficiently, and you bleed into the tissue (or out of an orifice if the vessel is there). It is also possible for someone with an MI that they have clots elsewhere in the body. Streptokinase could release tiny clots that then go on to block small vessels in the brain- the clots then rupture these vessels leading to a cerebral hemmorhage.

And the 'thinner' blood means that it is not clotting off the ruptured vessel effectively- not that the blood is 'thin' so it seeps out somehow.

 

[ohyeahbaby]

http://www.medscape.com/viewarticle/463997_3
About halfway down.

Any small vessel at any given time in your body is prone to a small tear/bleed due to high pressure or stress or weak architecture or infection or remodelling or whatever, and they are normally repaired efficiently so you never notice. If you are on an anticoagulant, these tiny tears are not able to be repaired efficiently, and you bleed into the tissue (or out of an orifice if the vessel is there). It is also possible for someone with an MI that they have clots elsewhere in the body. Streptokinase could release tiny clots that then go on to block small vessels in the brain- the clots then rupture these vessels leading to a cerebral hemmorhage.

And the 'thinner' blood means that it is not clotting off the ruptured vessel effectively- not that the blood is 'thin' so it seeps out somehow.

thank you BOTH! the article was long as s.hit but definitely worth the read, and StIGMA, I appreciate your explanation. It's exactly what I was looking for. Thank you.