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Male Speaker 1: This is Dr. Tom DeLauro who is going to be speaking about DVT prophylaxis, professor from the New York College of Podiatric Medicine.
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Male Speaker 2: Thank you very much. It's the bottom of ninth inning, the bases are loaded. It's too out. The last batter approach is the box and that would be me. So thank you for your patience and for being here. I would like to introduce this topic by telling you a true story of a patient who had chronically swollen limbs. Both legs were chronically swollen. One day one limb becomes more swollen than the other. The family is cognizant of DVT. They know what it is, so they asked the provider, do you think this might be that condition? The provider says absolutely not and gives the entire list as to why that canât be the case. The patient's family as the symptoms worsen -- the patient's family brings the patient to the emergency department where after she signs in at the registration desk, falls back dead from a massive pulmonary embolism. The coroner's report said it was a fatal pulmonary embolism that emanated from the deep veins of the leg. So in trying to defend this, we were asked several questions, such as did the provider meet the standard of care in assessing this patient's risk for developing a DVT? And second, were appropriate measures taken to prevent it? I have no disclosures and our current understanding of thrombosis, we need to thank this young man. Dr. Virchow's triad is true even till today and he postulated that thrombosis was the result of one of three factors that you see listed here that can occur singly or in combination with one another. But these next three slides will show you how they can interplay and how we can interpret each of these three things differently. For instance, we can think of abnormal blood flow as venous stasis secondary to being on a plane ride for too long or sitting in a car for too long. We can think of hypercoagulability as both inherited in a patient who test positive for factor V Leiden or acquired in someone who has antiphospholipid syndrome. And even something like inflammatory bowel disease can lead to hypercoagulability and vascular wall injury. We asked our students and residents to remember all these possibilities through the mnemonic I AM CLOTTED where I stands for immobilization, A for arrhythmia, M for myocardial infarction, C for history of hypercoagulability, L for longevity, O obesity, T for trauma and second T for tobacco, E for estrogen use and lastly history of prior deep venous thrombosis. But the question is who is at greater risk? Is it the older obese patients or is it the young girl who smokes and takes oral contraceptives? How do we answer that? We look to our friends from the American College of Chest Physicians and we looked to their point system that you may see in place at your hospitals. As we go through this point system, consider for a moment the patient you may see tomorrow or the surgery you have scheduled for later on this week and how many points do you think your patient would earn? You get one point somewhere between 41 and 60 years, minor surgery, history of major surgery within a month, pregnancy or having delivered a child within a prior month, history of varicose veins, inflammatory bowel disease which was a surprise to me -- I didnât know how that played in -- history of swelling of the legs, obesity, oral contraceptives which includes patches and hormone replacement therapy, post total hysterectomy. .
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Two points; older than 60 years -- I'm in that category -- malignancy or current chemotherapy or radiation, major surgery or tourniquet time longer than 45 minutes were all there, confined to bed longer than 72 hours, immobilizing cast shorter than a month. Three points; older than 75 years, history of DVT or pulmonary embolism, family history of thrombosis, factor V Leiden or activated protein C resistance and a medical patient with the risk factors of myocardial infarction, CHF or COPD and lastly congenital or acquired thrombophilia. The last category five points for each of these; hip, pelvis or leg fracture within one month, you may be called in a polytrauma case, stroke within a month, multiple trauma within a month. Look at the increase in risk when you just add a few more points. It increases exponentially, something to keep in mind. So now that we've talked about the when, what about the what. How do we take care of these patients and what's available to us? For lower risk patients, clearly everyone recommends early and aggressive mobilization, get out of bed as soon as you can, wiggle your toes, flex the ankle up and down, everything to keep the ankle pump moving. Next mechanical methods like graduated compression stockings or intermittent pneumatic compression devices, but keep in mind that these are effective only as adjunctive measures. And while they may be effective in reducing the incidents of distal thrombi, more proximal thrombi, ones that break off an emboli, they're not reduced. Here is group comparing relatively equal numbers of patients, those taking warfarin and those using IPCs. At the total at the bottom, relatively same number of thrombi. Look at the IPCs, very few in the calf, the popliteal with the plantar space but most of them were iliac and femoral; just the reverse on the patients who were taking warfarin. So there is a limit to what this can do, how much it can help us. After early mobilization and mechanical methods, what's next left, a pharmacological method. I throw [Indecipherable] [07:49] in a side before we move on. There was a recent report this past January of patients who were taking rosuvastatin having a decreased incidence of venous thromboembolism. So I asked that you just got to put that in the back of your head. Itâs a drug thatâs commonly used and maybe to your benefit in lowering the incidence of this particular problem. Before we go on to understanding the pharmacological methods a bit more, we have to take a few seconds and review blood clotting. What happens when a vessel is torn is immediately platelets start to adhere and form a little plug to close the hole. That and the fact that collagen fibers in the vessel wall are now free lead to a series of cascades, chemical cascades that ultimately convert prothrombin to thrombin and fibrinogen to fibrin. And it's that fibrin that forms a mesh that reinforces the plug that was created by the platelets. So when we look at the pharmacological methods, there is some new terminology, like some of these drugs will act at the level of platelet; we call these obviously antiplatelet drugs. Some will work on the chemical cascade; and these are called anticoagulants. Finally, some affect the generation of thrombin directly and these are called antithrombotics. So let's move through what's available to us and we'll talk about each one in turn. When I was a student, I did not like this chart. So we're going to suffer through it one more time. When the injury occurs within the vessel, that launches the intrinsic pathway. When the injury occurs outside the vessel, that launches the extrinsic pathways and they come together around Factor X in to the common pathway.
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The first drugs are the platelets active ones. Things like aspirin, COX-1 like ibuprofen and naproxen and lastly clopidogrel. They work at the level of where that red arrow is, thatâs how they work. Next, we look at the Coumarins. The first, platelet active drugs were oral. The Coumarins are also oral and they interfere where the green arrow is at the interaction between vitamin K and Factors II, VII, IX and X. The problem is that it takes about 36 to 72 hours for them to have an effect and the response is variable from patient to patient. And they need to be monitored and we looked to have an INR up to somewhere between 2 and 3. So because it takes time, we need to start them usually the night before the surgery. Next group are the heparins. These we need to subdivide into standard unfractionated versus lower molecular weight heparins. Heparins are given parenterally either IV or subcutaneously and actually have two properties. They're antithrombotic where the red arrow is and that they inactivate thrombin and they were also anticoagulant because they work with circulating antithrombin-3 to inactivate Factors IIa, Xa, IXa and XIIa where the navy blue arrow is showing. There are drugs that are specific for Factor Xa where the heavy navy blue arrow is. Fondaparinux, rivaroxaban and apixaban. We're seeing lots of commercials about these particular drugs and we'll talk about them how one compares with the other in a moment. There are direct thrombin inhibitors, really only one right now dabigatran. So how do they compare one with the other? Let's kind of walk through each column together. I got to learn how to do this -- there we go. We have aspirin and COX-1 that are platelet active, given orally, no monitoring is required, but you can't give them by themselves. And usually they're given at a dose thatâs much lower than one to exert any anti-inflammatory effect. The Coumarins are anticoagulant. They interfere with the cascade of events. Orally, they require monitoring of the INR and have a delayed onset of action; we spoke about that. Heparins are these next two columns, the unfractionated heparin and the low molecular weight heparin which is the one you're most familiar with, I'm sure; enoxaparin and dalteparin are anticoagulant and antithrombotic. They have to be given parenterally, but thatâs where they stop looking alike. The unfractionated heparins have to be monitored through an activated partial thromboplastin time, getting it up to 1.2 to 1.5 normal. It's a short half life only an hour. So the dose is usually every eight hours and there is a fairly high 8% to 15% chance that your patient will hemorrhage as a result of your therapy. In 2% to 4% of patients, they develop heparin-induced thrombocytopenia. So we have to watch for this by drawing platelet counts on day 3 and day 10 and looking for a drop of 50% or more in the platelet count which means this drug has to be withdrawn immediately. Factor Xa inhibitors are fondaparinux, rivaroxaban and apixaban; all antithrombotic. Whereas fondaparinux has to be given subcutaneously, rivaroxaban and apixaban can be given orally. Fondaparinux, you need to have a creatinine clearance of 30 mL per minute or more. So the kidney function has to be good enough, but no monitoring is required for rivaroxaban and apixaban. If I keep saying that over and over again, I'm sure I'm going to get tongue tied. Fondaparinux, given subcutaneously, rapid onset, long half-life, 18 hours, but there is an increased chance of bleeding. So normally it's started six to eight hours postop whereas rivaroxaban and apixaban decrease bleeding.
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And the notes are similar to what we see for enoxaparin, superior in that it can be given orally instead of it being given parenterally. Finally, dabigatran which is a direct thrombin inhibitor, orally, no monitoring, about as good as enoxaparin and approved by the FDA for deep venous thrombosis prophylaxis in 2015. So the bottom line again from the American College of Chest Physicians is this. No matter what you do, anything you use for 10 to 14 days postop is better than nothing at all. Anything is better than nothing. When using low molecular weight heparins, start 12 hours either pre or postop. It doesn't seem to matter. Of course, they're favorite over other agents and while an inpatient, usually the use of intermittent compression devices and antithrombotics are recommended over everything else. Continuing if the bleeding risk is high, then intermittent compression devices or no prophylaxis is recommended over all the pharmacological agents. Patients who refuse compression devices or injections than use the oral agents. In Europe, what's interesting is they usually prophylax 10 to 12 hours preop. In North America, we do 12 to 24 hours postop. Under the rule of never order a test you don't need because you get a result you don't want, if the patient is asymptomatic, do not order Doppler ultrasound before discharge because you'll be chasing after thrombi that you could have left alone. One of my daughters is a DPM and she was kind enough to research this and find this point system for me from the University of Michigan Health System. To kind of summarize as many of the things that we spoke about where -- here I go again -- this is the box for one point, you subtotal two points, subtotal three points, subtotal and of course five points. What's interesting is that the most frequently missed risk factor is the family history of thrombosis. So if you don't ask that now, you should. Make that part of your history before you do anything else. Patients may not be candidates for anticoagulant therapy and compression devices should be considered instead if they have a risk of increased bleeding. Patients may not be candidates for sequential compression devices if they have the history of severe PAD, CHF or acute superficial venous thrombosis. At least in the University of Michigan, this is how they take care of their patients depending upon the points that the patient acquires. Low, very low or early ambulation, we mentioned that. One to two points, use of sequential compression device. Three to four points, sequential compression devices or actually just one of these. So you can use sequential compression device or heparin or enoxaparin. But five or more points, the risk is high. They want compression devices plus heparin or enoxaparin. I found that a great reference for this was an article in Medscape in September of 2016, Deep Venous Thrombosis Prophylaxis in Orthopedic Surgery and outlines most if not all of the things that I mentioned this morning. With that, I thank you for your attention. Have a safe trip home.
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