Aspirin for DVT?

[DwayneEMTP]

So, after 5 days of traveling I've finally made it to my camp in PNG.

For the first time in ages I actually slept for about 8 hrs straight on my international flight...That flight lasted about 17hrs preceded by a ton of doing nothing. I'd medicated, as I always do, with 650mg ASA prior to flying.

Walking across the airport to get my next ticket in Brisbane I noticed sort of a sharp cramp in my right calf. I noticed at the time that it seemed strange that the 'cramp' was so localized, but it soon resolved so I didn't pay it much mind. I noted it in my head that a cramp after so many days of travel should cause me to focus on my hydration, which I'm pretty aware of at all times because of my travel, where I live and where I work.

Approximately 1.5 inches below the inferior edge of my patella and one inch beyond the medial line to the back it felt like I'd been hit with the round side of a ball peen hammer a few days ago, leaving an uncomfortable bruise. About where I'd expect the popliteal vein to be. (Googling later showed this to be the most common place for a leg DVT secondary to travel.) There is no one here to examine it so before Googling I tried to carefully get a baseline of area, tenderness, and pain level which I called a 3/10 at rest, 4/10 with palpation.

Later that day I arrived at camp and noticed that the pain at the site of the 'cramp' was getting worse. Maybe a solid 4/10 at rest, though nowhere near needing to be mitigated. Very localized

I called on of our online docs (we have a center with this company that have several medical directors online at all times) and explained the issue including my concern about a possible, and seemingly more likely DVT. She said that it sounded more like muscle strain and that she would call back the next day to check.

Out of concern for a DVT I took 600mg ASA 3x/day (no idea what an ideal dose would be, if there is one) in the hopes that if it was a DVT perhaps the antiagreggation qualities of the ASA would keep it from getting any bigger before we figured out what was going on.

They called back and said that after further consideration that they wanted me to go to the local hospital (5hrs by jeep) and get it checked out. I refused, as I'd have to pay for it, and it turned into a giant pissing contest.

During that contest I said, " So if we accept that I'm not going to go to the hospital until our confidence is higher that it's a DVT, what about continuing to medicate with ASA to try and keep it from getting bigger if it is?"

At this point it was getting difficult to walk without a limp, though still not a terribly big deal.

She said, "Mr Shithead (not what she said, but I could tell what she meant) you need an anticoagulant, ASA is not an anticoagulant. That means that it won't dissolve a blood clot..."

I said, "Yeah, I know what it means. But what I'm wondering is that for now I just have pain, no significant swelling, no measurable localized fever, why can't I use the antiagreggation from the ASA to try and maintain this state until my body dissolves the clot on it's own, assuming symptoms don't increase?"

"Mr Shithead! It's a blood clot! ASA will not dissolve it! You need to be seen at the hosptial!" Blah, blah, blah...

So I did it my way, wrapped my leg lightly with an elastic bandage before bed, the pain increased to a solid 5-6/10 later in the night though still without noticeable local fever or significant swelling or redness, until it suddenly, softly, 'popped' (Which my mind translated into a killer embolus breaking free, heading for my lungs) and decreased by about 50%, then over the next day resolved to complete resolution other than 2/10 pain with deep/aggressive palp.

So, after all of that, half of which I'm sure you wisely skimmed over...does it sound like a possible DVT? I'm about 50/50.

Also, I'm afraid that I'm a long ways out from A&P now with few opportunities to even think of clotting factors, cascades, etc, so I don't see what was so wrong with my plan assuming that we remove the non emergent transport to a 3rd world ER from the equation?

Understand that I would not have been happy with this plan if this had been my patient, nor confident enough to go forward with it, but this is me, so I was willing to be a bit more cavalier. Not stupidly so I think, but more so.

If the symptoms are caused by a clot, and the symptoms are relatively minor and appear to be doing no permanent damage, causing pain only, why would trying to keep the clot from growing further with ASA until my body could deal with the clot be such a stupid idea?

I'm sure it probably is...but I'm not sure why?

[Kiwiology]

You're making me think ... why must you make me think?

Aspirin as you rightly said is an anti platelet aggregator, it is not an anti thrombolytic. If you think you have DVT you need an anti thrombolytic.

Aspirin is helpful for somebody whose coronary artery occlusion ruptures because the damaged endothelium attracts platelets, which aspirin prevents. That is different than somebody with e.g. DVT or acute ischaemic stroke. They need thrombolysis.

Hope that helps, sorry I can't really be arse'd getting all the micro details in right now, I'm off to find me some Weet Bix ....

[BEorP]

Hey Dwayne, I suspect that what the doctor meant was that aspirin only deals with platelets rather than the actual clotting factors. If I recall correctly, once the coagulation cascade gets going, the platelet aggregation doesn't have anything to do with anymore.

I don't really know about whether there is "growth" of DVTs and what (if anything) anything could help in the situation you describe, but I don't think aspirin would be much use.

[chbare]

The doctor was right. Aspirin does not have much of a place in the treatment of DVT in many guidelines. Prevention is somewhat debatable however.

[paramedicmike]

From Tintinalli's Emergency Medicine:

"Patients with DVT complain of extremity pain, swelling *OR* cramping (emphasis mine)... About one quarter of patients with DVT have tenderness and redness in the swollen extremity, findings that are similar to cellulitis."

Wells Score, based simply on what you posted, would put you in the "moderate risk" category for DVT.

So it sounds like you needed to be evaluated for a DVT to me. Long international flight followed by pain in your calf? It could've been a cramp. It could've been dehydration. It could've been a DVT. Had you presented to me like that, on the phone or in person, I'd have worked you up for one. I understand you're dealing with a third world ER. If an ultrasound (if available) determined you had a clot then heparin would be the treatment. Aspirin wouldn't do much.

f the symptoms are caused by a clot, and the symptoms are relatively minor and appear to be doing no permanent damage, causing pain only, why would trying to keep the clot from growing further with ASA until my body could deal with the clot be such a stupid idea?

Because the threat from the clot breaking free, regardless of its size, is enough. That clot doesn't need to get bigger to break free. All it needs to do is shed a piece big enough to travel to your lungs, your heart or your brain and that's it. Sure, ASA may keep it from getting bigger through its antiplatelet properties. But getting bigger isn't the threat. The mere fact that its there, if it is a clot, is the threat.

And not to be a dick, but I wonder what your family would think about you being so cavalier with your health. Do you think they'd be as comfortable with your decision to not seek evaluation or treatment given the fact that you were evidently concerned enough about it to post a question here?

[Happiness]

Shithead ;(

[Arctickat]

Hmm, isn't there a lymph node in that anatomical area? What you're describing to me actually sounds like it might have been a lymphatic cyst.

[mobey]

Yeah man, I am with the Doc's here.

i fully understand that you know the ASA is not breaking down the clot. But I am unclear as to why exactly you are taking it?

Perhaps you think it will stop further clotting? Or prevent any new clots? Either way, you know it does not hold water.

I am also concerned the dose you are taking may result in further complications over any significant amount of time.

You are much like me. A terrible self-helth advocate.

If this were one of your patients, What would you recommend to them?

Go get this one dealt with, then concentrate on preventing them in the future.

You old guys gotta take these things more seriously

Edited July 15, 2012 by mobey

[DwayneEMTP]

But what I don't understand is what makes at DVT special? We get clots all the time don't we? I mean in A&P we had to learn every step of the clotting cascade, creating and destroying clots, though as should be obvious by now the retention of that material was abysmal. Surely I didn't need to learn all of that for an issue that is rare except in DVT, stroke?

And yeah, that is my thought, and I get that it's dumb, but I'm still not clear on why it's dumb. Risky maybe, I get that, but why is the theory poor?

Don't we give ASA to MIs stop the aggregation, (in my mind, further development of the clot, so maybe that's where I'm lost) of the clot? To queer it's further growth until we can get them to a higher level of treatment for dealing with the existing clot? I can see thrombotics there as time is of the essence, but if it wasn't, wouldn't the body deal with that clot in it's normal way, assuming that the acute cause of the clot development had been removed, as it had been with my international flight/dehydration?

And if the body is regularly building and destroying clots due to injuries both minor and severe that aren't treated with thrombotics, then why does waiting for my body to destroy this clot, if preventing it's growth is possible, seem so off in the ditch?

And I don't know that stopping this clot or preventing further clots doesn't hold water. Not being pissy, just honest. I have taken ASA before my international flights for a long time...grin...for just that reason. Now I'm starting to feel a bit silly about that...

I really, really want to just Google this, but then I lose the opportunity to build a decent logic tree for this issue.., so I'll take my beating, and gladly, so don't worry that you'll hurt my feelings....I just don't get it.

And no worries Mobes...before long your pubes will sprout and give you a whole new outlook on life and respect for your elders... :-)

[BEorP]

Don't we give ASA to MIs stop the aggregation, (in my mind, further development of the clot, so maybe that's where I'm lost) of the clot? To queer it's further growth until we can get them to a higher level of treatment for dealing with the existing clot?

Hey Dwayne, My understanding is that the ASA prevents the development of further clots but doesn't prevent further development of the clot. So that current clot is what it is, but at least we can reduce the chance of more forming before someone can fix it. If it works so well for MIs, maybe the ASA could have been good if someone were at risk of multiple DVTs concurrently? (No idea how common that is...) Still though, ASA won't touch the current clot. Once the clotting factors get going, they do a whole lot of amplification on their own and platelet aggregation doesn't have much to do with it as far as I recall. ASA only affects the platelets but has no impact on the actual clotting factors.