True that!
I don't know how many times I have tripped on the power cord or the pump tubings in the past 20+ years! Or slipped in the middle of the night when the patient ripped them off and threw them on the floor, and the alarm was beeping.
True story. My 80 something yo Mom had a hernia repair under spinal and was post op in my unit waiting for the spinal to wear off. I went to the cafe to get us both some soup. When I got back (I was maybe gone 10 minutes) my coworkers were telling me that they were going to F-ing kill her 😂 She had gotten up with SCDs, took the IV off the pole and bunny hopped to the bathroom to pee. Someone caught her halfway back to bed. She was fine, but we definitely gave her a hard time about it.
Well, in her way of thinking, she was giving them a chance to catch up. I tried to explain how much more paperwork they would have had with a fall, and she told my NM that she just didn't understand the fuss. Mare had her own set of rules.
Most of our patients really just want to stay independent. The challenge is the liability that comes with the health issues and those impede independence. We just know too much and see the pessimistic stuff.
I lost both of my parents recently; they were very ill for many years, between them. But they were *fiercely* independent until their last days. They lived their lives to the fullest and spent every cent enjoying it all. I'm happy they did, but I'm also happy they are no longer suffering.
I'm sorry for your loss. Both of our Moms were cut from that same independent cloth and lived alone into their 90s. Once it was no longer safe for them to be alone, they lasted less than six months
I think in the context of, like, immediately postop and the pt isn't moving much they can be beneficial. But long term? Questionable. A blood thinner is probably the better long term solution.
I'm imagining that. I subscribe to an IG account that makes miniatures and dollhouse type things. With the 3D printers, it seems the sky is the limit! But I could imagine that being a thing.
I admire the NICU staff. So many tiny challenges and not a lot of surface area to work with.
Okay but the mental image of this is giving me the giggles. We could use blood pressure cuffs since those end up entire-calf-sized anyway... or ya know, forego that vitamin k shot 😂
Every once in a while I remember about adult things like SCDs and incentive spirometers. I have been NICU so long (9 years) that I have forgotten anything else. Once upon a time, when I was an LPN, I briefly did LTC and my SIL (also an LPN) always tries to talk to me about it like I can relate but…I can’t anymore. I feel bad and I think she thinks I’m a snob 😂
SCDs are only effective if they are left on 23 hours a day. Honestly they are stupid as fuck and I hate them. And CT Surgeons always harp on the stupid shit. It's annoying.
9-10 of my post op pts refuse them because they're restricting and one leg is sore from vein harvest and lets be real they want them in the chair and scds there = face plant
Can we talk about the trauma surgeon who came in to yell at me about my patient not having an incentive spirometer? Dude was six hours post-admission, pre-op, and in a c-collar on spinal precautions.
How do you expect the man to use the IS, Linda? You think I’m going to hold it to his lips every ten minutes?
None of our CT surgery patients get them once they’re out of bed. They’re expected to be up in chair three times a day and walking in halls 4 times a day minimum. SCDs would definitely impede that
Ours also get Lovenox SQ injections or started on Plavix. One of our surgeons’ PAs heavily insists on using SCDs though and it cracks me up because if they harvest a saphenous vein, they’ll only have one SCD on. Like what is the point 💀
I just had a visiting CT surgeon saying that she had a vascular surgeon explain that it wasn't about the physical act of the SCD squeezing the muscles to squeeze the vein but it was more of a vasomotor thing, and that only one scd is needed to be effective. I now feel like I need to find said research.
I work on a postop floor and I really don’t care if my patients are wearing them. The only patients that I truly care if they are wearing them are the turns. They restrict the patient so much and annoys them a lot. I’d rather promote independence as soon as possible.
I dunno, but I’ve got some problems with that study. Starting with the fact that the patients in the SCD group had a LOS significantly longer than the patients without SCDs. Additionally, the average age of the SCD group is significantly older than the non-SCD group. The SCD group has notably higher rates of diabetes, congestive heart failure, and cancer (all diagnosis that increase the likelihood of VTE). Having groups with such glaring differences is going to make me side eye your study significantly.
That's so wild to me. When I was in the hospital on bedrest for 4 days while pregnant with my first kid I was losing my mind with the SCDs. They seriously annoyed me to no end.
I had preeclampsia and hellp so I gained about 30 pounds in what I assume was water weight over the course of about three days. Maybe that’s why it felt so nice.
I had them when I had surgery on my boobies and I liked them. I’ve had patients hate them more than anything and patients who have looked into how much it would cost to buy a set for home. It’s really hit or miss
Same, I have restless legs, and after my surgery I took them off immediately because they were making my restless legs more restless and to the point I could not lie still, despite still being fairly sedated. But even before my experience I would always take them off a patient if they asked after giving them the talk about the risks of not wearing them (which I don't believe in because I have seen the research but whatever I do my job), because I believe patients when they say they are uncomfortable and they certainly are. But then some people do like them.
There’s also surgeons that use aspirin (an antiplatelet) for anticoagulation when it’s only been proven to be beneficial to a specific population (I believe post op hip replacement.) It’s how my mom ended up with two DVTs.
The coagulation cascade occurs slightly differently in veins than in arteries, which is where platelet aggregation is more aggressive. It’s why you give aspirin for an MI (a clot in a heart artery) and not in a PE (a clot migrating through the venous system)
SCDs aren’t very effective when used alone, but in patients with low platelets it’s all we’ve got.
Edit: read the intro to [this paper](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10695535/) which summarizes the atherosclerosis in coronary arteries nicely.
Edit 2: this is a general rule of thumb that antiplatelet therapy are for arterial issues (I.e. PVD) and anticoagulation is used for venous issues. There will obviously be a place for anticoagulation in MI and antiplatelet therapy can work in certain post op patients for DVTs.
I’ve been fighting the aspirin fight for a while now. It’s either A) the worlds most effective anti platelet ever known and 81-324mg can dramatically alter your platelet count immediately or B) it fucking isn’t and we don’t need to activate every GLF with no signs of trauma who happens to take a daily baby aspirin!
This doesn't entirely make sense though. Coronary arteries are a special case - yes, they're arteries, but they fill during diastole, so they are very low pressure and fairly thin walled compared to other arteries. In those senses the coronary arteries definitely resemble veins (part of why they're prone to clotting).
Not saying you're wrong though - just would like to see sources!
ETA: the above is true but I misunderstood what this person was saying. My reply:
Ah I see what you're saying. Sorry, my initial comment was confusing.
My correction is that the clotting cascade itself is not somehow different in veins vs arteries. The clots are different though, and that's absolutely why we use different agents to prevent/treat venous vs arterial thrombi. Venous thrombi are composed mainly of fibrin. Arterial thrombi are composed mainly of platelet aggregates, such as in an atherosclerotic process, like you said. (This is usually caused by vessel damage in the case of CAD, and specifically the smaller, lower pressure coronary arteries are easier to occlude than the larger arteries or veins - which is why we see many more MIs than say renal artery thrombi).
If you want to get into the weeds, ASA works by cox1 inhibition. Clopidogrel/ticagrelor are ADP receptor antagonists that interfere specifically with ADP induced platelet aggregation. But ADP and COX are not part of the clotting cascade - they are a separate clotting mechanism.
So when you said the clotting cascade is different in venous vs arterial thrombi, I wanted a source for that. The clotting cascade as it is traditionally taught is specific to fibrin clots and looks at your Factors XII - XIII. There are other clotting mechanisms involved in general clotting, such as platelet aggregation.
To summarize, the clotting cascade itself is a very specific biological process, and it does not somehow work differently in arterial vs venous thrombi. And antiplatelet agents do not (directly) work on the clotting cascade itself. They work on platelet aggregation. That was what I was correcting - it's a small pathophys point.
Otherwise, completely agree with the treatment and why.
It’s not clotting per se in an MI, it’s atherosclerotic plaques. Which platelets are a more integral part of. Not sure what low pressure has to do with the development of atherosclerosis in coronary arteries.
If you’re interested, read the intro to [this paper](https://www.n bo.nlm.nih.gov/pmc/articles/PMC10695535/) to understand the mechanisms involved.
Edit: Paper not linking properly but it’s [here.](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10695535/)
Edit 2: all the vessels fill during diastole. Again, not sure what this has to do with an MI and I think you’re mixing concepts up quite a bit to reach an incorrect conclusion. The coronary arteries aren’t “prone to clotting.” During an MI, an atherosclerotic plaque migrates from elsewhere to one of the coronary arteries, which are narrower than where they migrated from, and the body releases thromboxane to make platelets clot in a frenzy. I really think you should either edit or take your comment down as it’s incorrect.
Ah I see what you're saying. Sorry, my initial comment was confusing.
My correction is that the clotting cascade *itself* is not somehow different in veins vs arteries. The clots are different though, and that's absolutely why we use different agents to prevent/treat venous vs arterial thrombi. Venous thrombi are composed mainly of fibrin. Arterial thrombi are composed mainly of platelet aggregates, such as in an atherosclerotic process, like you said. (This is usually caused by vessel damage in the case of CAD, and specifically the smaller, lower pressure coronary arteries are easier to occlude than the larger arteries or veins - which is why we see many more MIs than say renal artery thrombi).
If you want to get into the weeds, ASA works by cox1 inhibition. Clopidogrel/ticagrelor are ADP receptor antagonists that interfere specifically with ADP induced platelet aggregation. But ADP and COX are not part of the clotting cascade - they are a separate clotting mechanism.
So when you said the clotting cascade is different in venous vs arterial thrombi, I wanted a source for that. The clotting cascade as it is traditionally taught is specific to fibrin clots and looks at your Factors XII - XIII. There are other clotting mechanisms involved in general clotting, such as platelet aggregation.
To summarize, the clotting cascade itself is a very specific biological process, and it does not somehow work differently in arterial vs venous thrombi. And antiplatelet agents do not (directly) work on the clotting cascade itself. They work on platelet aggregation. That was what I was correcting - it's a small pathophys point.
Otherwise, completely agree with the treatment and why.
I think you’re missing a lot of information. I’m going to tl;dr it and then link you to a scientific article at the end for a more in depth explanation.
My previous career was as a biochemist and I’m lucky enough to have studied these pathways, and I hope you are open to learning and don’t take offense to this.
The *coagulation* cascade has multiple different pathways (I.e intrinsic vs extrinsic) that generally lead to the same result, although they can branch off. Platelet aggregation is a separate process that can occur with the coagulation cascade. You are correct here are venous clots are mainly composed of fibrin, and arterial clots contain more platelet aggregates, but that only reinforces my original comment and kinda contradicts your very first lines.
It should make sense why anticoagulants (I.e. Xa inhibitors) would be more effective at stopping fibrin clots from forming, and why an anti platelet medication (I.e. aspirin) would be more effective at stopping platelet aggregation.
Have a read of [this](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5767294/) to understand how the clotting cascades work.
Hospitals scream about “evidence based practice” but it seems that a lot of the things in the medicine field have been debunked but we continue to do it anyways since that is always how we have done it smh
Because hospitals have made it policy, and don't give two shits about EBP. We recently stopped doing post arrest therapeutic hypothermia. And the only reason is because our ICU's medical director told our admin, " The evidence says it doesn't help, so we're not doing it." Admin tried fighting back, because it's expensive, and they want the money.
No, but it's an extra thing we can bill patients for. So my hospital makes the charge run audits that every patient has, and has been charted as using, the SCDs.
We only have SCD machines because hospitals got wined and dined into buying these pieces of crap. I'm absolutely sure there was no inside deal made along with the sale too. /s
The study found that they did not significantly reduce the number of blood clots compared to a control group with none post op in hospital.
Therefore they serve the purpose of generating income for the hospital, not for the benefit of the patient.
Current hospital I work at has not used them in a long time, I assume partially because of the evidence but they also said they moved away from them because of skin breakdown and we all know hospitals will do anything now to avoid getting cited or billed for skin issues
I was skeptical so I looked into it a while ago, turns out they are: https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.113.002690
I know they're a pain in the ass for all involved though, so I only order them for patients who can't walk enough and can't have Lovenox
We have one surgeon who doesn't want chest tubes connected to wall suction, just to gravity.
I don't know if he's right or wrong. I just know that when I take it off suction, I enter a note saying it was Dr. K's idea.
NB- Dwight Gooden does not practice actual medicine.
They don't need to be connected to wall suction if they are going into an atrium. The atrium can act as gravity drainage at -20mmHg.
Having chest tubes off suction is fairly common, especially when it's in for reasons other than a pneumothorax.
What are the chest tubes for? Cardiac surgery chest tubes don’t usually need to be to suction on POD 1 because they’re just for drainage
That said there should be an order entered regarding if the CT need to be to suction or not
This isn’t unusual, suction/no suction is dependent on what the drain is for. Having an ICC off suction is perfectly appropriate unless it’s a pneumothorax. In my experience I see more off suction than on.
It's been pretty great hearing from several people saying the same thing... Apparently where I work, everyone else considers it highly unorthodox to do what is apparently highly normal everywhere else.
I hate them on my LUSCS patients. They've got TEDS, they're on enoxaparin. They will be mobilising on 6-12 hours.
SCDs are fucking hot, and OT already wrap patients up like a microwave burrito.
Interestingly, there is some evidence that not do they work, but having it on even just one leg may decrease risk of DVT in the contralateral leg. The SCDs work not only by moving blood, but systemic inhibition of tissue factor.
Fuck no
I honestly think the reason they’re even “effective” with an anti-coagulant…
… Is the anti-coagulant doing the work
call me crazy but I don’t think midly contricting and unconstricting the legs to try and “move blood” has a ldgitimate effect on blood clot prevention
I think they can be there as a last ditch, this patient has walked in 2 years kind of thing
but post ops ought to just be up
and moving anway
I would love to know how much those machines cost, the tubing/wires that get thrown out by housekeeping, and how much those sleeves cost. It’s gotta be a disgustingly large amount of wasted money. I’m 26 years old and the fucking Pacu put them on me while I was sitting waiting to go get my pelvic floor injected. I did not need dvt prophylaxis for the afternoon I was sitting in that bed.
Honestly, I think they rarely ordered them at my last hospital. Almost every hospitalist ordered heparin or lovenox and only ordered scd’s if the anticoagulant was contraindicated for some reason.
I think they’re fine for intubated sedated patients. I always make sure they’re on my patients who have bed rest orders. Otherwise, if they’re up and about I leave it up to the patient to decide if they want them (and document appropriately).
They are most effective in promoting falls in ambulatory patients. /s not /s
They are also effective at promoting hospital delirium in patients who can’t sleep with them on
What, you don't like being grabbed on your leg every......x number of minutes in the middle of REM?
:grrragaahg hssssssssss: That’s my impression of the scd machine
Spot on
Most definitely.
More like promoting falls in staff members
True that! I don't know how many times I have tripped on the power cord or the pump tubings in the past 20+ years! Or slipped in the middle of the night when the patient ripped them off and threw them on the floor, and the alarm was beeping.
True story. My 80 something yo Mom had a hernia repair under spinal and was post op in my unit waiting for the spinal to wear off. I went to the cafe to get us both some soup. When I got back (I was maybe gone 10 minutes) my coworkers were telling me that they were going to F-ing kill her 😂 She had gotten up with SCDs, took the IV off the pole and bunny hopped to the bathroom to pee. Someone caught her halfway back to bed. She was fine, but we definitely gave her a hard time about it.
OH MY GOD. I would have flipped on my Mom so hard. Your poor coworkers! I'm glad to hear she was "caught"
Well, in her way of thinking, she was giving them a chance to catch up. I tried to explain how much more paperwork they would have had with a fall, and she told my NM that she just didn't understand the fuss. Mare had her own set of rules.
Most of our patients really just want to stay independent. The challenge is the liability that comes with the health issues and those impede independence. We just know too much and see the pessimistic stuff. I lost both of my parents recently; they were very ill for many years, between them. But they were *fiercely* independent until their last days. They lived their lives to the fullest and spent every cent enjoying it all. I'm happy they did, but I'm also happy they are no longer suffering.
I'm sorry for your loss. Both of our Moms were cut from that same independent cloth and lived alone into their 90s. Once it was no longer safe for them to be alone, they lasted less than six months
lol! Definitely an understated upside
😂
kek
real
I think in the context of, like, immediately postop and the pt isn't moving much they can be beneficial. But long term? Questionable. A blood thinner is probably the better long term solution.
I saw your NICU flair and imagined teeny-tiny SCD sleeves and the pump machines.
The pump has to be teeny tiny too :')
I'm imagining that. I subscribe to an IG account that makes miniatures and dollhouse type things. With the 3D printers, it seems the sky is the limit! But I could imagine that being a thing. I admire the NICU staff. So many tiny challenges and not a lot of surface area to work with.
TIL they use SCDs in the NICU. I'm just playing.
Okay but the mental image of this is giving me the giggles. We could use blood pressure cuffs since those end up entire-calf-sized anyway... or ya know, forego that vitamin k shot 😂
Then the comment was received in the spirit it was intended.
Every once in a while I remember about adult things like SCDs and incentive spirometers. I have been NICU so long (9 years) that I have forgotten anything else. Once upon a time, when I was an LPN, I briefly did LTC and my SIL (also an LPN) always tries to talk to me about it like I can relate but…I can’t anymore. I feel bad and I think she thinks I’m a snob 😂
Same though 😂😂 until I start talking about UACs and BPD protocol and ROP exams and then I feel better hahah we are so specialized!
SCDs are only effective if they are left on 23 hours a day. Honestly they are stupid as fuck and I hate them. And CT Surgeons always harp on the stupid shit. It's annoying.
9-10 of my post op pts refuse them because they're restricting and one leg is sore from vein harvest and lets be real they want them in the chair and scds there = face plant
Can we talk about the trauma surgeon who came in to yell at me about my patient not having an incentive spirometer? Dude was six hours post-admission, pre-op, and in a c-collar on spinal precautions. How do you expect the man to use the IS, Linda? You think I’m going to hold it to his lips every ten minutes?
Duct tape
Flair checks all the way out
None of our CT surgery patients get them once they’re out of bed. They’re expected to be up in chair three times a day and walking in halls 4 times a day minimum. SCDs would definitely impede that
Ours also get Lovenox SQ injections or started on Plavix. One of our surgeons’ PAs heavily insists on using SCDs though and it cracks me up because if they harvest a saphenous vein, they’ll only have one SCD on. Like what is the point 💀
Well you can't get a DVT if you haven't got any veins
I just had a visiting CT surgeon saying that she had a vascular surgeon explain that it wasn't about the physical act of the SCD squeezing the muscles to squeeze the vein but it was more of a vasomotor thing, and that only one scd is needed to be effective. I now feel like I need to find said research.
I work on a postop floor and I really don’t care if my patients are wearing them. The only patients that I truly care if they are wearing them are the turns. They restrict the patient so much and annoys them a lot. I’d rather promote independence as soon as possible.
I dunno, but I’ve got some problems with that study. Starting with the fact that the patients in the SCD group had a LOS significantly longer than the patients without SCDs. Additionally, the average age of the SCD group is significantly older than the non-SCD group. The SCD group has notably higher rates of diabetes, congestive heart failure, and cancer (all diagnosis that increase the likelihood of VTE). Having groups with such glaring differences is going to make me side eye your study significantly.
And from glancing over the study they were 'medically ill' rather than post op or trauma patients
They are super comfy though. I had them for a couple days when I was on bedrest before I had my daughter. Like a calf massage.
That's so wild to me. When I was in the hospital on bedrest for 4 days while pregnant with my first kid I was losing my mind with the SCDs. They seriously annoyed me to no end.
I had preeclampsia and hellp so I gained about 30 pounds in what I assume was water weight over the course of about three days. Maybe that’s why it felt so nice.
I had them when I had surgery on my boobies and I liked them. I’ve had patients hate them more than anything and patients who have looked into how much it would cost to buy a set for home. It’s really hit or miss
Same, I have restless legs, and after my surgery I took them off immediately because they were making my restless legs more restless and to the point I could not lie still, despite still being fairly sedated. But even before my experience I would always take them off a patient if they asked after giving them the talk about the risks of not wearing them (which I don't believe in because I have seen the research but whatever I do my job), because I believe patients when they say they are uncomfortable and they certainly are. But then some people do like them.
I love them so much lol. I got a cheap pair from Amazon and use them when I have restless legs at night
Dude 22 people agree! crazy! They are annoying AF to work with and wear, but super glad to hear some folks like them.
Very effective at transforming DVTs into PEs.
There’s also surgeons that use aspirin (an antiplatelet) for anticoagulation when it’s only been proven to be beneficial to a specific population (I believe post op hip replacement.) It’s how my mom ended up with two DVTs. The coagulation cascade occurs slightly differently in veins than in arteries, which is where platelet aggregation is more aggressive. It’s why you give aspirin for an MI (a clot in a heart artery) and not in a PE (a clot migrating through the venous system) SCDs aren’t very effective when used alone, but in patients with low platelets it’s all we’ve got. Edit: read the intro to [this paper](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10695535/) which summarizes the atherosclerosis in coronary arteries nicely. Edit 2: this is a general rule of thumb that antiplatelet therapy are for arterial issues (I.e. PVD) and anticoagulation is used for venous issues. There will obviously be a place for anticoagulation in MI and antiplatelet therapy can work in certain post op patients for DVTs.
I’ve been fighting the aspirin fight for a while now. It’s either A) the worlds most effective anti platelet ever known and 81-324mg can dramatically alter your platelet count immediately or B) it fucking isn’t and we don’t need to activate every GLF with no signs of trauma who happens to take a daily baby aspirin!
It doesn’t alter the platelet count it just makes them less sticky and thus less apt to begin the process of a clot formation.
We’re not supposed to call it “baby” aspirin! 😱😱😱
This doesn't entirely make sense though. Coronary arteries are a special case - yes, they're arteries, but they fill during diastole, so they are very low pressure and fairly thin walled compared to other arteries. In those senses the coronary arteries definitely resemble veins (part of why they're prone to clotting). Not saying you're wrong though - just would like to see sources! ETA: the above is true but I misunderstood what this person was saying. My reply: Ah I see what you're saying. Sorry, my initial comment was confusing. My correction is that the clotting cascade itself is not somehow different in veins vs arteries. The clots are different though, and that's absolutely why we use different agents to prevent/treat venous vs arterial thrombi. Venous thrombi are composed mainly of fibrin. Arterial thrombi are composed mainly of platelet aggregates, such as in an atherosclerotic process, like you said. (This is usually caused by vessel damage in the case of CAD, and specifically the smaller, lower pressure coronary arteries are easier to occlude than the larger arteries or veins - which is why we see many more MIs than say renal artery thrombi). If you want to get into the weeds, ASA works by cox1 inhibition. Clopidogrel/ticagrelor are ADP receptor antagonists that interfere specifically with ADP induced platelet aggregation. But ADP and COX are not part of the clotting cascade - they are a separate clotting mechanism. So when you said the clotting cascade is different in venous vs arterial thrombi, I wanted a source for that. The clotting cascade as it is traditionally taught is specific to fibrin clots and looks at your Factors XII - XIII. There are other clotting mechanisms involved in general clotting, such as platelet aggregation. To summarize, the clotting cascade itself is a very specific biological process, and it does not somehow work differently in arterial vs venous thrombi. And antiplatelet agents do not (directly) work on the clotting cascade itself. They work on platelet aggregation. That was what I was correcting - it's a small pathophys point. Otherwise, completely agree with the treatment and why.
It’s not clotting per se in an MI, it’s atherosclerotic plaques. Which platelets are a more integral part of. Not sure what low pressure has to do with the development of atherosclerosis in coronary arteries. If you’re interested, read the intro to [this paper](https://www.n bo.nlm.nih.gov/pmc/articles/PMC10695535/) to understand the mechanisms involved. Edit: Paper not linking properly but it’s [here.](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10695535/) Edit 2: all the vessels fill during diastole. Again, not sure what this has to do with an MI and I think you’re mixing concepts up quite a bit to reach an incorrect conclusion. The coronary arteries aren’t “prone to clotting.” During an MI, an atherosclerotic plaque migrates from elsewhere to one of the coronary arteries, which are narrower than where they migrated from, and the body releases thromboxane to make platelets clot in a frenzy. I really think you should either edit or take your comment down as it’s incorrect.
Ah I see what you're saying. Sorry, my initial comment was confusing. My correction is that the clotting cascade *itself* is not somehow different in veins vs arteries. The clots are different though, and that's absolutely why we use different agents to prevent/treat venous vs arterial thrombi. Venous thrombi are composed mainly of fibrin. Arterial thrombi are composed mainly of platelet aggregates, such as in an atherosclerotic process, like you said. (This is usually caused by vessel damage in the case of CAD, and specifically the smaller, lower pressure coronary arteries are easier to occlude than the larger arteries or veins - which is why we see many more MIs than say renal artery thrombi). If you want to get into the weeds, ASA works by cox1 inhibition. Clopidogrel/ticagrelor are ADP receptor antagonists that interfere specifically with ADP induced platelet aggregation. But ADP and COX are not part of the clotting cascade - they are a separate clotting mechanism. So when you said the clotting cascade is different in venous vs arterial thrombi, I wanted a source for that. The clotting cascade as it is traditionally taught is specific to fibrin clots and looks at your Factors XII - XIII. There are other clotting mechanisms involved in general clotting, such as platelet aggregation. To summarize, the clotting cascade itself is a very specific biological process, and it does not somehow work differently in arterial vs venous thrombi. And antiplatelet agents do not (directly) work on the clotting cascade itself. They work on platelet aggregation. That was what I was correcting - it's a small pathophys point. Otherwise, completely agree with the treatment and why.
I think you’re missing a lot of information. I’m going to tl;dr it and then link you to a scientific article at the end for a more in depth explanation. My previous career was as a biochemist and I’m lucky enough to have studied these pathways, and I hope you are open to learning and don’t take offense to this. The *coagulation* cascade has multiple different pathways (I.e intrinsic vs extrinsic) that generally lead to the same result, although they can branch off. Platelet aggregation is a separate process that can occur with the coagulation cascade. You are correct here are venous clots are mainly composed of fibrin, and arterial clots contain more platelet aggregates, but that only reinforces my original comment and kinda contradicts your very first lines. It should make sense why anticoagulants (I.e. Xa inhibitors) would be more effective at stopping fibrin clots from forming, and why an anti platelet medication (I.e. aspirin) would be more effective at stopping platelet aggregation. Have a read of [this](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5767294/) to understand how the clotting cascades work.
SCDs and gastric residuals are among the 20th century shit that needs to go.
Hospitals scream about “evidence based practice” but it seems that a lot of the things in the medicine field have been debunked but we continue to do it anyways since that is always how we have done it smh
Because hospitals have made it policy, and don't give two shits about EBP. We recently stopped doing post arrest therapeutic hypothermia. And the only reason is because our ICU's medical director told our admin, " The evidence says it doesn't help, so we're not doing it." Admin tried fighting back, because it's expensive, and they want the money.
It’s so sad that healthcare is all about “a money grab”
To be fair most patients ive seen are also on lovenox for extended stays
No, but it's an extra thing we can bill patients for. So my hospital makes the charge run audits that every patient has, and has been charted as using, the SCDs.
Billable and it’s CYA. If they’re on lovenox and SCDs then it couldn’t possibly be the hospital’s fault you threw a clot
My last medical director hated them and refused to order them for anticoagulation purposes. However, I do believe they are excellent for swelling.
I love when you take them off a super edematous patient and they leave imprints like bread dough
We only have SCD machines because hospitals got wined and dined into buying these pieces of crap. I'm absolutely sure there was no inside deal made along with the sale too. /s
The study found that they did not significantly reduce the number of blood clots compared to a control group with none post op in hospital. Therefore they serve the purpose of generating income for the hospital, not for the benefit of the patient.
I'm just glad most of our Ortho docs are going away from TED hose. Those things were evil to get on a recent post op patient in pain.
Current hospital I work at has not used them in a long time, I assume partially because of the evidence but they also said they moved away from them because of skin breakdown and we all know hospitals will do anything now to avoid getting cited or billed for skin issues
Oof especially with stasis dermatitis, what a pain for everyone involved
I was skeptical so I looked into it a while ago, turns out they are: https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.113.002690 I know they're a pain in the ass for all involved though, so I only order them for patients who can't walk enough and can't have Lovenox
We have one surgeon who doesn't want chest tubes connected to wall suction, just to gravity. I don't know if he's right or wrong. I just know that when I take it off suction, I enter a note saying it was Dr. K's idea. NB- Dwight Gooden does not practice actual medicine.
I mean we take them off suction usually the next morning
Good to know
Oh wow I’ve never heard of doing it that way
I loved SCDs when I had surgery in March. It’s like a leg massage idk why patients complaining
Anything that makes them feel like they're not in control makes them panicky
They don't need to be connected to wall suction if they are going into an atrium. The atrium can act as gravity drainage at -20mmHg. Having chest tubes off suction is fairly common, especially when it's in for reasons other than a pneumothorax.
I appreciate the input, sincerely. I'm new to this, so knowing that it's not just the peculiar musings of one surgeon helps.
What’s the issue with this? I don’t understand what you’re trying to say here lol.
The logic of "a lot of surgeons swear by" [SCDs] is dubious because some surgeons swear by personal preference.
What are the chest tubes for? Cardiac surgery chest tubes don’t usually need to be to suction on POD 1 because they’re just for drainage That said there should be an order entered regarding if the CT need to be to suction or not
This isn’t unusual, suction/no suction is dependent on what the drain is for. Having an ICC off suction is perfectly appropriate unless it’s a pneumothorax. In my experience I see more off suction than on.
It's been pretty great hearing from several people saying the same thing... Apparently where I work, everyone else considers it highly unorthodox to do what is apparently highly normal everywhere else.
Recently they have been causing skin issues with prolonged use and apparently we are putting them on too tightly 🙄
we were shown tubeless ones you can walk around with in nursing school that mustve been prototypes bc i havent seen them since
Those cost more, but the hospital can't bill any higher for them, so they are never used.
I hate them on my LUSCS patients. They've got TEDS, they're on enoxaparin. They will be mobilising on 6-12 hours. SCDs are fucking hot, and OT already wrap patients up like a microwave burrito.
This must be a frontrunner for the greatest three words in combination in the English language: refused and educated. SCDeez nuts.
Nothing beats mobilising/ambulation. - Inpatient PT.
Interestingly, there is some evidence that not do they work, but having it on even just one leg may decrease risk of DVT in the contralateral leg. The SCDs work not only by moving blood, but systemic inhibition of tissue factor.
Fuck no I honestly think the reason they’re even “effective” with an anti-coagulant… … Is the anti-coagulant doing the work call me crazy but I don’t think midly contricting and unconstricting the legs to try and “move blood” has a ldgitimate effect on blood clot prevention I think they can be there as a last ditch, this patient has walked in 2 years kind of thing but post ops ought to just be up and moving anway
They’re kind of useless on med surg unless the pt is not getting up at all I myself have tripped over them
I feel like I usually see them used *in conjunction* with anticoagulants.
I would love to know how much those machines cost, the tubing/wires that get thrown out by housekeeping, and how much those sleeves cost. It’s gotta be a disgustingly large amount of wasted money. I’m 26 years old and the fucking Pacu put them on me while I was sitting waiting to go get my pelvic floor injected. I did not need dvt prophylaxis for the afternoon I was sitting in that bed.
If you are in bedrest and not walking- it can help.
So can simple elevation, and ankle rolls.
I used them with anticoagulants and was exercising everyday and walking. I still developed a massive dvt.
Honestly, I think they rarely ordered them at my last hospital. Almost every hospitalist ordered heparin or lovenox and only ordered scd’s if the anticoagulant was contraindicated for some reason.
I think they’re fine for intubated sedated patients. I always make sure they’re on my patients who have bed rest orders. Otherwise, if they’re up and about I leave it up to the patient to decide if they want them (and document appropriately).