foreign what's up Ninja nerds in this video today we're going to be talking about Venus thromboembolism that includes dvts and PES let's begin our discussion talking about the pathophysiology of dvts or deep vein thromboses so when we talk about this the pathophysiology is obviously there is a clot a thrombus that develops within the veins and what veins well usually it's the veins of the legs that are most commonly affected let's pretend that we have a very simple diagram here of the inferior vena cava and then down here we go into the iliac veins what if
you had a little clot in that area that could be an iliac DVT if you go down a little bit further and we got the femoral vein that if I got a clot in there that could be a femoral DVT I get down to the popliteal vein it could be a popular deal DVT I get down to the peroneal veins that could be a peroneal DVT oftentimes we make this a lot simpler and we say that anything that's usually Above This bifurcation so popular femoral iliac I have what's called a proximal DVT and then if
it's below that it's called a distal DVT so that's really important to remember same thing tibial veins if you get a clot there tibial DBT so tibial and perone are more distal dvts for moral popularity on iliac or more of the proximal dvts so the question is when the heck is causing these veins to become thrombotic and really this comes back to that concept of Virgos Triad so virko's Triad says that if their stasis of blood flow there's hypercoagulability or endothelial injury you can increase the risk of a clot let's go through each one of
those stasis what is this this is usually where there is increased amount of time for the platelets to bind with the endothelium and lead to a clot so what are some things that can cause stasis it's pretty straightforward right post-op states where patients are kind of bedridden for a bit paralysis where they can't move and therefore that's another reason or really really long travel greater than eight hours at least in a plane or car look for that in the clinical vignettes that's a big one the other one is that there's destruction of the endothelium the
endothelium is normally supposed to release things like nitric oxide prostacycline that blocks platelets from binding but if you have endothelial injury now the plates can just stick right away so what are some things that basically does that well it could be things like smoking that's a really big risk factor surgical procedures but the biggest one I really want you to watch out for is if they have venous catheters especially like femoral central venous catheters that can definitely cause this other one is hypercoagulability this is basically where you have an increase and the number of pro
coagulants things that want to cause clotting and a decrease in the number of anticoagulants the things that want to prevent clotting and that's the concept here so what are some of these things that can cause this well let's talk about it you know patients who develop malignancy like in pancreatic cancer or in lung cancer they can increase the amount of pro-coagulants which will then lead to a clot formation other scenarios would be if they have situations of pregnancy or their own oral contraceptives please don't forget that one it definitely can increase their pro-coagulant production another
one is if they have mutations particularly something like Factor five Leiden or prothrombin gene mutations this can also increase the amount of pro coagulants that they form when there's decreasing anticoagulants that's the same fact you have less of these things to prevent clotting usually there's less protein C less protein s less antithrombin three what if I pee a bunch of them out like a nephrotic syndrome that could also cause this another one is if they have anti-phospholipid syndrome usually this is a patient who has an underlying history of Lupus but they have these antibodies called
anticardial Lipan antibodies that lead to the decreased production of these different types of anticoagulants so that's another one so look for patients with SLE and positive anticardial lip and antibodies another one is they're on Heparin and patients who take Heparin this may seem super paradoxical when they take Heparin some patients develop a reaction to the Heparin and they produce particular molecules like platelet Factor fours and these different types of antibodies that bind onto the Heparin and then what happens is this leads to clots that are forming all over the place that consume a lot of
your platelets and some of your clotting proteins and then the patients also bleed so this is another really big thing to watch out for is heparin-induced thrombocytopenia now with that being said we have an understanding of the reasons why the patients may form clots in their veins whether it's the proximal or distal veins causing dvts but the question then leads to what is the ways that these patients will present if they have a clot in their veins well you're preventing venous flow and so it backs up and it causes a lot of pain and swelling
of the leg and sometimes if you do this special test where you try to have them dorsiflex you try to push that it'll cause a lot of pain it's called a positive home inside should be careful with that because it can't actually break the clot off and lead to a PE but these are the big things to remember here for DVT all right so why is a DVT so bad what's scary about it well there's a couple things one is it can cause a lot of congestion of blood so if you can't move blood especially
with a really proximal DVT like an iliofemoral one that's really really proximal the blood will back up and it'll cause the limb to become super congested and become a bluish limb appearing and so we call that phlegmasia cerule dolans sometimes if the congestion is so bad it can actually cause compression of the nearby artery which reduces blood flow to the actual Limb and you'll start getting a white pale limb which we call phlegmasia Alba right dolans and so think about albinos right the next thing is that sometimes after they have the clot and then they
actually maybe they they get put on anticoagulants and the clot dissolves sometimes the actual vessels have this thing called A post-thrombotic syndrome and that's usually where the veins are just not very good at being able to move blood properly and they can develop peripheral vasculars disease or chronic venous insufficiency as a result the last and probably the scariest complication of a DVT is if that clot pops all the way up goes up into the right atrium right ventricle pulmonary artery and gets stuck there and causes a pulmonary embolism this can lead to decreased blood flow
the lungs which can lead to pulmonary failure and it can also have less blood leaving the heart which can lead to heart failure and potentially put a patient into shock so how do we diagnose a DVT well if a patient comes in and they have leg swelling edema a positive Homen sign they have history that suggests that they would have some of the Virgos Triad features stasis of blood flow hypercoagulability or some type of endothelial injury then you should go ahead and consider that and ways that we do that is we look at the Wells
score and it says okay do they have any previous DVT because that puts them at a high risk active cancer hypercoagulability recent embolization or a bedridden stasis localized tenderness along the venous distribution that again suggests more of a DVT leg swelling suggests DVT asymmetric calf swelling pitting edema collateral superficial non-varicose veins and an alternative diagnosis you subtract points away so based upon this you'll kind of gather up all your points and say which one did this patient have if you do this and you generate a very low score like I'm talking like you know less
than one or maybe even you get a couple like you get like score of one to two this means your pre-test probability is like it's really low so there's not a guarantee that this patient has a DVT but you're pretty you're I'd say you're pretty confident that it's a low likelihood of DVT what you can do is you can obtain a d dimer this is a molecule that's basically indicative of maybe potential clots that are forming it's not super specific though but it may be somewhat helpful if the D-dimer is really low you can say
with a decent amount of confidence that the DVT is not likely there and you can exclude the diagnosis if it's greater than 500 though then you can't necessarily exclude the diagnosis so you may have to move on to the next step which is to obtain an ultrasound of that actual area that appears to be swollen or look or rule out a DVT in the iliac femoral tibial popular area the other thing is if your score is greater than two so they have a score that is at least greater than two then you can say okay
I got a high probability that I have a DVT I'm not even going to waste time on a D-dimer I'm going straight to getting an ultrasound so low probability moderate probability obtained D-dimer if it's positive and it's elevated go to get an ultrasound if it's a high probability don't waste your time with a D-Day armor just go right to an ultrasound from there if the ultrasound shows that they have a DVT Boom the diagnosis is confirmed you got a DVT and you find out where it is is it proximal or distal if it's negative then
again you've ruled out the DVT and so this is the way that I would want you guys to remember about going about diagnosing a DVT use the Wells Criteria don't go crazy in memorizing this try to understand the actual pathophysiology of how dvts form and the presentation of dvts and you'll be pretty good to go here but again if they were to do this they would give you these scoring systems and help you to determine what's the next step give me a D-dimer or give me an ultrasound all right how do we treat a DVT
it's actually pretty straightforward if it's a massive proximal DVT where the patient has that findings of phlegmasia ceruleodolans or alidons you got to get on this man because these are super high risk kind of dvts and you should do a thrombectomy sometimes you can consider a little bit of intra-arterial TP or intravenous TPA to go into the air like catheter directed so you take a catheter you go into that area of the vein and you squirt a little TPA in there but generally like a thrawn back to me would be preferred if it's a proximal
DVT without findings of phlegmasia cyrilla dolans then oftentimes it's just anticoagulating them but if they have a contraindication to anticoagulation then you might have to do an IVC filter and then lastly if it's a distal DVT you want to then consider do I really need to anticoagulate these patients you can but some you can just observe and you can repeat it with an ultrasound and see if the actual DVT has gotten bigger there is these like small criteria I don't want you guys to go too crazy with it but a distal DVT you could consider
anticoagulating or you could observe it with a repeat ultrasound and see if it gets bigger and extends into one of those proximal veins then I would anticoagulate the patient all right I think one of the biggest things to remember is that you want to figure out why the patient has the DVT because you can put them on anticoagulation you can do a thrombectomy you could serial ultrasound them but you want to figure out what was the reason they developed a DVT and try to prevent that from occurring another DBT all right we'll move into the
next component here which is when that DVT that clot breaks off moves up and gets stuck in one of the pulmonary arteries now we have a pulmonary embolism so when a pulmonary embolus forms there is many different causes and the way that you can remember this is the mnemonic fatal fat embolus air embolus thrombus like a DVT amniotic ambolus or less common the septic emboli so again that's going to be the big things to remember here the classic way that these patients will present is they may have pluritic chest pain they may have dyspnea they
may have hemoptysis but again remember this mnemonic it's fatal fat embolus air embolus thrombus amniotic and less common out of all of these the DVT is by far going to be the most common cause of a PE okay fat embolus would be if you have a big old like long bone fracture air embolus is if you're performing some type of procedure like a central venous line and you end up actually getting a little bit too much air that gets kind of shot into the veins amniotic embolus could be during the actual birthing process and if
a patient has a history of infective endocarditis that's affecting the tricuspid valve that could also break off and block the actual blood flow but these are the big things here to remember okay oftentimes I would say that the most common finding that these patients have of a pulmonary artery embolus is usually dyspnea so that's the big one to remember I can't honestly say I've ever seen a patient with hemoptysis or pleuritic chest pain distance definitely is going to be one of the most common findings all right with that being said if a patient has a
pulmonary embolism why are these things so bad and so terrifying I'd say one of the biggest things is respiratory failure think about it you have a block of blood flow from the pulmonary artery to the lungs you can't perform gas exchange you're going to have a poor perfusion and therefore you're going to have a normal ventilation or increased ventilation so because of that there is a VQ mismatch that'll lead to hypoxemia so again normal ventilation poor perfusion you get a VQ mismatch hypoxemia the patient and a result of the hypoxemia can develop an increase in
their heart rate this is one of the classic findings as a patient who has dyspnea hypoxemia tachycardia and maybe they're working a little bit harder to breathe they're to kipnik their dyspneck and that is really big signs to look for so if a patient comes in they have signs of dyspneum they're working a little bit harder to breathe their respiration rate is increased they have a low O2 saturation and they have a sinus tachycardia with a recent diagnosis of a DVT you better be thinking about a pulmonary embolism that's causing respiratory failure okay the other
thing that's probably the most terrifying thing is obstructive shock if you have a really large saddle embolus that's blocking blood flow I'm going to have almost no good blood flow leaving the right ventricle the resistance the blood flow is going to be so high because of that my right ventricular afterload is going to be really high I'm not going to be able to get blood out of my right ventricle so it'll start to fail and it'll dilate when it dilates and it fails to get blood flow moving forward blood will back up and they'll develop
jugular venous distension on top of that their RV will dilate and it'll start shifting things from the right to the left if I do that I reduce my amount of blood flow that can come into the left ventricle because I'm Shifting the septum and that'll reduce the cardiac output that'll cause the patient to have a rebound tachycardia hypotension and sometimes they can even go into shock I've seen a lot of patients just go into pea rest from a massive saddle embolus so I think some of the biggest things to watch out for if a patient
has a pulmonary embolus is to watch out for sinus tachycardia tachypnea complaints of dyspnea hypoxemia and then watch out for hypotension these are the big things that you really want to watch out for all right how do we approach a pulmonary embolism if a patient comes in they have dyspnea they have tachycardia they have work of breathing they have hypoxemia they have hypotension with some of these findings and a history of a DVT I'm going to get it first a chest x-ray and ECG this may sound dumb because you're like how am I going to
be able to diagnose a pulmonary embolism off this anytime a patient has dyspnea or any kind of chest pain or they have any hypoxemia you should always get these tests a chest x-ray can at least rule out other things like pneumonia or pulmonary edema Etc so usually it's normal that's one of the biggest things that you want to remember is a chest x-ray is usually completely normal the EKG is actually somewhat helpful for your boards not helpful in true real life though but you're going to find a couple things one of the things that they
like to say is the S1 Q3 T3 this is usually a sign of right heart strain so if you look for a ripe bundle branch block right Axis deviation and you see a Q wave and Lead one you see inverted T waves and Lead three and he also again see this potential right Bumble branch block these are usually potential signs that a patient may be having right heart strain so again S waves and Lead one Q waves and Lead three inverted T waves and Lead three and a right bundle branch block and if they also
have right Axis deviation which they do also have right Axis deviation here where their Q their S Wave is really deep in lead one and then they have a Big R wave and Lead three this is definitely right Axis deviation right bundle branch block S1 Q3 T3 all signs of right heart strain because you can't get blood out of the right heart into the pulmonary because of the embolus but by far the most common finding is usually sinus tachycardia if you get lucky you may see the S1 Q3 T3 by far the most common finding
is sinus tachycardia all right from here if you have a normal chest x-ray an ECG that suggests right heart strain or sinus tachycardia think about what's the chances that they have a pulmonary embolism so you do that Wells Criteria scoring do they have any features of DVT is there another diagnosis that makes this potentially you know another alternative is their heart rate greater than 100 beats per minute do they have sinus tachycardia potentially now if they had any immobilization or recent surgery would that increase their risk of that varicose Triad do they have a history
of dvtpe do they have hemoptysis do they have malignancy these are all things again I want you to think about where malignancy is suggestive of a hypercoagulable condition immobilization is consistent with stasis hemoptysis could be a potential complication tachycardia is a potential sign that there is hypotension or respiratory failure and then again features of a DVT history of a dvtp if you do this and you get your score and it shows that it's less than two it's low low low risk so I want to go even a little bit further and really make sure that
I don't miss a pulmonary embolism so if I do my well score it's less than two I'm going to do another score that really will help me to rule out a pulmonary embolism this is called a perk score a pulmonary embolism rule out criteria and it just looks at their age their heart rate their saturation if they have any hemoptysis private PE DVT leg swelling recent surgery trauma or estrogen use if there is not one point that I get out of that it's not a PE but if there is at least one point at least
one or greater I cannot safely send that patient home with confidence saying that they do not have a PE so if their perk score is greater than or equal to one or they have a moderate probability so a score of greater than two at least two to six from here I'm going to get a d dimer because again it's indicative of maybe that there's a lot of clot burden if the D-dimer is less than 500 I can pretty much confidence say okay it's unlikely to be a PE or DVT if the d uh D-dimer is
greater than 500 that's a decent amount and that's relatively concerning and I can't with good strength and good kind of like cognitive like power say I can send this home patient without send this patient home without ruling out of PE so then from there I will move to the next test and that's going to be a CT pulmonary angiogram or a VQ scan I would also order this test if they have a very high probability so high probability of a PE you go right to the best test ctpa versus EQ scan moderate probability D dimer
if they have a very low probability use the perk score if the perk score is zero it's included if it's greater than or equal to one D dimer if dime is greater than 500 ctpa or VQ scan now which one would I actually get here the CT pulmonary angiogram or the VQ scan it depends upon the patient do they have some type of contrast algae or a very terrible kidney disease are they pregnant and these um sorry if they have contrast allergies or if they have some type of like terrible like disease of their their
um kidneys I probably wouldn't want to do a CT pulmonary angiogram and I prefer a VQ scan but most cases the ctpa is the preferred test it'll basically help me just look at the pulmonary artery and say oh there she blow there's this death clot that I can see here whereas a VQ scan it can help me to see potentially areas of perfusion defects by these web shaped kind of markings you see here here's the ventilation here's the perfusion you can see in these particular areas there's no perfusion that's going to these particular areas so
that could also help me to diagnose a PE with that being said if it does not show a PE on the p uh the ctpa or the VQ scan I've excluded a PE but if I do see a p then I have to ask myself the question is there a submassive or low risk p e or a massive PE how the heck do I determine that all right get the echocardiogram if the echocardiogram does not show any RV dilation or RV dysfunction it is a low risk PE if it does show RV dilation or RV
dysfunction it is a submassive or massive PE and you're going to look here you're going to see this right heart look how big and dilated this is the right ventricle should not be bigger than the left ventricle over here so that's definitely RV dysfunction then I asked myself the question is the BP low if the BP is low that means that this is really a patient who's really bad and they have a massive PE burden and if it's normal then it's a sub mass of PE this is the ways that I want you guys to
think about how do we diagnose a PE all right I know this was a lot so now what I want to do is I want to say okay let's treat a patient who has a pulmonary embolism because it's going to kind of bring all these things together well the first thing is I have to ask the question are the hemodynamically unstable because if they are not hemodynamically unstable is it a low risk or a submassive PE it's both of those it would be a low risk or submasopee the difference is that a sub mass of
B is RV dysfunction low risbe has no RV dysfunction all right and the only way I'd be able to diagnose if they have a PE is a CT pulmonary angiogram or a VQ scan if they have a high probability I go straight to that if they have a moderate probability with a D-dimer than 500 I go to that if they have low probability perk score can't rule them out D-dimer get to the 500 I go to this scan either way I've gotten to the point where I say okay I got a submassive PE RV dysfunctional
blood pressure low risk p no RV dysfunction normal blood pressure what do I do well I ask myself the question do they have a contraindication to anticoagulation if there's no contraindication give them into coagulation Warfarin Heparin Xarelto apixaban I'm putting them on some type of anticoagulant if they do I cannot safely give them anticoagulation I got to put an IVC filter in to prevent further dvts from popping off and going up to the pulmonary artery if the patient is hemodynamically unstable and they have what's called a massive PE their blood pressure is low they have
RV dysfunction and I found that off the ctpa likely as the biggest one I asked myself the question do they have a contraindication to TPA if they do not give them TPA and if they do then you have to go in and do an envelectomy and that is the way that we would go in and diagnose a patient and treat a patient with a pulmonary embolism all right my friends The Next Step here is how do we prevent the venous thromboembolism well and patients who have this potential risk it's obviously treating their underlying cause right
but I think one of the biggest things is that if a patient's in the hospital I think you need to have pharmacological prevention especially in patients who are hospitalized they're immobile they're at their bed rest they have an increased risk of Venous stasis and can form a DVT so oftentimes we do what's called Low molecular weight Heparin or subcutaneous Heparin and this is usually going to be something that we will perform in a patient again we do this if they have no contraindication to this and they're hospitalized they're immobile and they're on bed rest if
a patient is immobile on bed rest and we cannot safely give them these anticoagulate kind of molecules here like low molecular weight Heparin or subcutaneous Heparin then we'll do these things these little devices these sleeves that we put on their leg and it'll intermittently kind of apply pneumatic compression to squeeze the actual legs and squeeze the veins to continue to keep moving and mobilizing blood and that's the big ways that we would actually go through understanding Veno thromboembolism ninjas I hope this made sense I hope that you guys enjoyed it as always until next time
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