• DVT Prophylaxis – Guidelines and role of compression

    Professor Ross Crawford

    Brisbane – Australia

    Date: 10/12/21
    Duration: 19:24 mins

    Abstract

    Explore the current concepts of deep vein thrombosis (DVT) and pulmonary embolism (PE) prophylaxis concentrating on the total joint replacement surgery – with Professor Ross Crawford Orthopaedic Surgeon Brisbane, Australia. Join Dr Crawford as he discusses the supportive evidence to find the fine balance between thromboprophylaxis and not having a significant systemic complication or the complication of an intra-articular bleed;

    Topics

    • guidelines for venous thromboembolism (VTE) prophylaxis
    • Incidence of VTE events
    • Prophylaxis options and their evidence
    • Dr Crawford’s preferences and supporting evidence

    Transcript

    My name is Ross Crawford.  I’m an orthopaedic surgeon in Brisbane, Australia.

    I have had a very very long term interest in the treatment or prevention or PE and DVT following joint replacement and hip fractures.  It has been a long battle and we have been long advocating for mechanical compression as an important part of the treatment.

    I am going to just discuss a little bit today about the guidelines for DVT prophylaxis and the role of compression.

    So the aim of today is to explore the current concepts in DVT and PE prophylaxis concentrating on the total joint replacement and mechanical compression.

    My belief, and it is a personal belief, is that the use of potent anticoagulants as DVT prophylaxis following surgery is unnecessary following total joint arthroplasty.  We must remember that the sale of potent anticoagulants such as the NOACs, Clexane and other potent anticoagulants is a multi-billion dollar industry and there is very strong industry interest in keeping us using these drugs for prophylaxis.

    What are we trying to achieve as joint replacement surgeons around an operation?  We are trying to prevent death including fatal PE and we are trying to prevent wound complications including bleeding, infection and haematoma and the truth is we can make patients bleed to death or we can make patients clot to death depending on what we actually did to them.  So it is that fine balance between thromboprophylaxis and not having a significant systemic complication and that complication of an intra-articular bleed and potentially a haematoma and an infection.  This is the thing you see when you use potent anticoagulants.  We can see skin necrosis, we can see secondary infection and often the need to go back and wash out a knee for infection.  So we have to be very cautious with being too aggressive with the use of potent anticoagulants.

    There are a number of guidelines around and the American Academy Guidelines in particular noted that major bleeding was very rare amongst patients receiving aspirin or mechanical devices.  They thought it was about .14% compared to more systemic interventions at 1.8%.  Again that is more than 10 times the risk of a major bleed if you use something more potent than aspirin.

    What about the incidence of VTE events?  DVT is probably common is you go looking for it but it is a pretty poor surrogate end point.  Because PE is rare, probably .1%, a maximum of 1% and fatal PE is even rarer.  The literature today would say it is probably less than 1:1000 probably closer to 1:10,000 cases.  So we are really not dealing with a common complication and we have got to bring that risk balance into the right level to match up our bleeding risk versus our clotting risk.

    If we look at the systemic review post VTE in Bangkok in 2011 they looked at 2,500 patients.  They actually went looking for it with DVT and venography and found around 31% of patients had clots but symptomatic DVT was 4.5%, the PE rate of .6% and the fatal PE rate was 0%.  So no fatal PEs.  So do not go looking for clots you will just get yourself into a world of hurt.

    So DVT is probably high if you look for it.  The background rates are falling with change in clinical practice.  We now mobilise our patients on the day of surgery or day following surgery so they are no longer sitting around for extended periods.  We are using tranexamic acid, we have minimal bleeding and we are very aggressive in localisation.  Remember that PE and fatal PE rates are very low and really interestingly some recent studies have shown that PE may be unrelated to DVT and this whole question of clot embolisation is even being questioned.  It may be that clots are in fact forming in the lung and they are nothing to do with the clots that are seen in the leg.

    What about mortality?  We really want to keep our patients alive and I do not think we can get away with it now but Bloom in 2006 did a study on 1800 patients in which they had no prophylaxis.  They had 17 deaths which gave them a 1% 90 day mortality and only 7 deaths or .4% by 30 days.  It is probably a bit higher than we would like and as I said I do not think the use of nothing is able to be justified in the current circumstances.

    But if you look at the cause of death in Bloom’s study, 7 or .4% were from ischaemic heart disease, 4 or .23% were cardiovascular events and only .12 or close to 1:1000 was actually from a PE.  So the mortality from pulmonary embolus even with no thromboprophylaxis is very low indeed and interestingly those ischaemic heart disease and cardiovascular events may well be protected by aspirin as we know it is cardioprotective and that might be the reason that it is such an effective agent at decreasing mortality.

    What about treatment?  So we have a number of choices with our treatment.  We can have early mobilisation, we can use spinal or epidural anaesthetic.  We can use mechanical compression and we can use some form of chemical thromboprophylaxis.  My choices are early mobilisation, spinal anaesthetic, mechanical compression including sequential compression devices and TED stockings and aspirin 100 mg/day for 6 weeks.  So are my decisions and choices rational?  Let us have a look at the supporting evidence.

    So the guidelines.  If we can go back to the American Academy.  There is no good evidence that early mobilisation works but the consensus of the Group was that early mobilisation following hip and knee arthroplasty is cost effective, there is minimal risk to the patient and is consistent with clinical practice.  The American Academy recommend the use of spinal anaesthetic in total joint replacement and there are very many reasons to do that.  It is vasodilatory, so we get less back bleeding and you certainly see decreased blood loss if you use a spinal anaesthetic.  There is, however, no hard evidence that spinal anaesthetic will decrease the risk of DVT or PE but it is certainly good on many levels.

    The American Academy recommend the use of pharmacological agents and/or mechanical devices for the prevention of venous thromboembolism in patients who just have the risk of the operation.  We are not going to go today into the Factor V leiden or more complicated patients but for a routine patient having total hip and knee replacement there is moderate recommendation to use both compression and mechanical devices.  And the chest physicians again agree that we should use dual prophylaxis with an antimicrobial agent and IPCD during the hospital stay.

    So what are the results of mechanical compression.  There is quite a historic study from Professor Ling in Exeter and I tend to quote this study because Professor Ling was my mentor and it was interesting that he was so far ahead of the game that he was actually using foot compression in the 1980’s without any chemical thromboprophylaxis.  They looked for blood clots and found 40% of the control group had DVT and only 5% in the compression group and in another study from 1999 looking at compression alone, Hooker et al found 4.6% DVT in no compression and .6% with compression.

    If we go to Korea, Kim et al in 2015 looked at 1400 total knee replacement patients with compression alone.  They found 6% DVTs on venogram which I certainly would not recommend to you but there were no symptomatic PEs on spiral CT scans.  So 0% PE rate and 0% mortality rate in a large series of patients.

    The Lancet interestingly had a study looking at patients who had a stroke.  They looked at a multi-centred randomised control trial.  They looked at almost 3,000 patients in 94 hospitals in the United Kingdom and they found a highly significant decrease in DVT when they used intermittent compression versus patients who did not.  They also found a decreased or cause mortality in patients who had intermittent compression.  So I think the orthopaedic community has probably led

    the world in the use of compression and I think the physicians and many of the other groups need to look at the literature and probably anyone in hospital who has decreased mobility should be getting some form of mechanical compression.

    What about the results of combined drug and compression.  If we go to the Cochrane database, which looked at a pool database, of all the systemic reviews in 2016 they found moderate evidence suggesting that combining compression and pharmacological prophylaxis was better than using either one alone and cumulatively they decreased the incidence of DVT and PE.

    Caccous et all 2012 did a metanalysis of 1400 patients and they found in total knee the DVT rate reduced from 18.7% when people just used anticoagulation to 3.7% when they used combined.  So you can see the very strong effect of mechanical compression.  In total hips they went from 9.7% down to .9% when compression was added to chemical prophylaxis.  So there is pretty clear evidence that the addition of IPC augments the efficacy of anticoagulation preventing DVT in THR and TKR.

    Manamadel, another study out of Asia, looked at fractured neck of femur patients and they randomised to pre-op compression or routine post-op compression and chemicals and found that compression and chemical gave a very low DVT and significantly decreased the combination from 7.4% to 3.7%.

    So what is mechanical prophylaxis.  People talk about it and it is a bit of a nebulous concept to many.  In broad terms it is any compressive device attached to the leg.  It can include compression stockings, intermittent pneumatic compression and foot pumps or so called foot impulse technology.  Compression stockings are Class 1 to 3, one is for prevention, 3 is for treatment of significant oedema or varicose ulcers.  They come in below and above knee forms.  Most use below knee and that certainly is my preference.  They are often not mentioned because most people use them as routine and the in hospital benefit may not be a DVT but in swelling reduction and at the moment it is a default mechanical treatment on discharge.

    There is a picture of above knee compression stocking, not at all as easy to fit as this leg would be and I must admit my patients, particularly in the Brisbane summer, are not enthusiastic wearers of compression stockings.

    Sequential compression is just that. It is a device that encircles the limb, inflates with distal to proximal and moves fluid form the venous system back towards the heart.  Foot pumps have a more rapid flow but are not as well tolerated by all so I do not have a strong preference as to foot pumps or pumps and sleeves.  But remember that all pumps and sleeves are not the same.  There are very different levels of technology, different levels of research and you need to ask your vendor to give you some evidence as to what their compression devices actually do.

    So my preference is below knee sequential compression devices but occasionally we use foot pumps in patients who have a preference.  The easy illustration of a compression device and on the next slide you can see how the foot pump technology work.  There is a home based monitor, the foot device and the cord that connects the two and the air is pumped sequentially.

    So when you are looking at a compression system you want to look at the total volume of blood moved, you want to look at whether you have sustained blood flow, you want to see if you have unidirectional blood flow, look for blood clearance from behind the valve cusp and peak blood flow.  All of these are important in the mechanism of prevention of DVT.

    Here are some pictures showing the uniform stress of one of the compression devices that you can see gives nice uniform compression around the limb and not all devices can achieve such as good effect.  And again you can see four different systems and one of the systems has a 7.8 l/hr flow and smallest is 3.3.  So more than double the effect with difference systems.   But ask your vendor as I said for some evidence around why you would choose their system.  And again you will see different studies showing different rates of DVT and different rates of PE.  So ask for literature.  It is a bit like a hip stem, not all hip stems are equal.  If someone said to you which hip implant are you going to use you would not just say I’ll use a hip implant, you would actually read about the implant, look for the evidence that supports it so do the same for with your compression device.  Actually look for the one that has clinical evidence to support it.

    How do they work?  They work in two ways.  One is probably inherently obvious and the other I think is even more interesting.  So they actually move the fluid from the venous system as we talked about and that improved flow prevents pooling in the vessels of the lower limb.  But more interestingly that sheer effect of rapid blood flow across the vessel wall has a fibrinolytic effect and probably creates a chemical environment that lowers the risk of blood clot and one fascinating study from years ago actually showed a compression device on the arm was able to decrease the risk of blood clots in the legs and that was purely a chemical rather than a mechanical effect.

    You can see in this video here that the valve here is open.  There is some blood pooled around the valve and momentarily you will see the valve close and you will see the effect of the compression as fluid is pumped through the valve and the valve then closes.  And this slide shows what happens at the vessel wall when you increase blood flow.  You get increased tissue plasminogen activator, increased tissue factor pathway inhibitor and the increased flow in strain and sheer across the blood vessel wall has a very very important effect on the chemical changes in the venous system and that I think is a very underestimated and understudied area of research.  Tissue factor pathway inhibitor inhibits Factor Xa and subsequently inhibits the Factor V IIa tissue factor complex.  So there are very logical reasons why this sheer force is so effective.

    Here is the complex clotting cascade the intrinsic and extrinsic system.  You can see where the intermittent pneumatic compression acts on the extrinsic system to lower the risk of clots.  And tissue plasminogen activator is a protein involved in the breakdown of blood clots and catalyses the conversion of plasminogen to plasma and it is the major enzyme responsible for clot breakdown.  So you can see anything that increases the levels of tissue plasminogen activator has got to be a good thing in preventing clots.  And prostacyclins give you platelet activation and are an effective vasodilators so we are acting on the platelets, we are acting on the vessel walls and we acting on the extrinsic clotting system.

    So in conclusion, every patient should have a properly fitted compression stocking and a customised mechanical pump and should start early/  We start on the non-operative limb in theatre and on the operative limb the compressive device is placed in recovery and the patient then has that for their entire journey through the hospital.  Which chemical is still open to debate.  As I said my preference is aspirin, that debate will be ongoing.  It is not really material to this talk around the use of mechanical compression because we have seen pretty clearly we are going to use mechanical and you are going to choose the chemical that you are most comfortable with and I think it is cost neutral or cheaper to use aspirin than certainly is to use low molecular weight heparins or the newer NOACs.

    Thank you very much.

    Professor Ross Crawford
    Prince Charles Hospital and QUT, Brisbane Australia

    Professor Crawford is an Orthopaedic Surgeon with a special interest in lower limb joint replacement; his principal interests are hip and knee replacement, and knee arthroscopy. Professor Crawford is an internationally recognized expert in the field of hip and knee replacement surgery. He performs approximately 150 hip and 150 knee replacements per year, both in public and private practice. He lectures and teaches surgical techniques both nationally and internationally.

    As well as running a clinical practice Professor Crawford has a chair of orthopaedic research at the Queensland University of Technology. In this role he supervises PhD students, a number of post-doctoral researchers and collaborates closely with experts in the field of tissue engineering, cartilage degradation, cartilage mechanics, and clinical orthopaedics. The research in the outcomes of surgery performed under Professor Crawford’s care is an important part of his research practice.

    Professor Crawford’s private surgery is performed at the Holy Spirit Northside Hospital. This hospital and the Prince Charles Hospital, where public surgery is performed, are on the same campus.