• Mako Virtual Range of Motion

    Styrker – Mako

    Date: 28/8/21
    Duration: 2:31 mins

    Abstract

    The virtual range of motion feature allows the user to visualise and assess impingement between the femur, the pelvis and their planned components during different patient manoeuvres.  Watch the virtual range of motion feature in action.

    Transcript

    The virtual range of motion feature allows the user to visualise and assess impingement between the femur, the pelvis and their planned components during different patient manoeuvres.

    In reduced mode a 3 x 2 table is displayed in the lower left hand side of the main window with columns labelled as stand and sit and rows labeled as flexion extension, internal external and abduction adduction.   When the user selects the stand or sit column labels, the patient pelvic bone model will update its orientation.  If pelvic tilt has not been input for either pose the supine pose will be assumed for the pelvic model during range of motion assessment.  If pelvic tilt values have been entered the virtual range of motion tool uses the pelvic tilt inputs for the stand and sit poses.

    The user can switch to a lateral view of the bone models by selecting the lateral view button in the control panel.  The table allows the user to modify range of motion values for the selected pose.  The entered values should approximate the maximum expected range of motion for the patient.

    The feature also allows the user to make adjustments in 5° increments by selecting either the up or down arrow next to each input box.  When the user changes the range of motion values for the operative femur and there is contact between bone models and/or implant components the application will provide visual feedback to notify the user.  The visual representation will be highlighted in red.

    To better assess impingement between components the user may need to rotate the view and hide the femur and stem models.  The surgeon can change the supine cup inclination or supine cup version in the reduced mode by entering the values in the input boxes to avoid impingement.

    Stryker Robotics Profile

    Mako SmartRobotics combines three key components: 3D CT-based planning, AccuStop haptic technology, and insightful data analytics, into one platform that has shown better outcomes for total knee, total hip and partial knee patients. It all starts with a CT scan that creates a 3D image of the patient’s unique anatomy. This information allows you to create your patient’s plan and assess and balance the joint. Using the CT scan of your patient, Mako AccuStop haptic technology guides you to cut what’s planned precisely for each patient. For some patients, that means preserving soft tissue; for others, that means saving healthy bone. Learn more about this technology and the surgical techniques.

  • 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.

  • Treatment of Intracapsular Hip Fractures – Current practice

    Professor Ross Crawford

    Brisbane – Australia

    Date: 10/12/21
    Duration: 12:42 mins

    Abstract

    Treatment of intracapsular hip fractures (not sliding hip screws or intramedullary nails) inregards to patients who require some form of arthroplasty for their hip.  Be that a hemiarthroplasty or a total hip replacement. The objectives are to examine the guidelines around hip fracture treatment, understand the role of cement in the treatment of femoral neck fractures, to study the safety or not of cement and to learn the technique of cementing in hip fracture patients.

    Transcript

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

    I have had a long term interest in the management of hip arthritis and the fixation and treatment of fractured neck of femurs.  I also have an academic role at the Queensland University of Technology.

    Today we are going to talk to you about the treatment of intracapsular hip fractures.  We are not going to discuss sliding hip screws or intramedullary nails we are just going to talk about patients who require some form of arthroplasty for their hip.  Be that a hemiarthroplasty or a total hip replacement. The objectives are to examine the guidelines around hip fracture treatment, understand the role of cement in the treatment of femoral neck fractures, to study the safety or not of cement and to learn the technique of cementing in hip fracture patients.

    Firstly we will run through some guidelines from America and the UK, we will look at some trends and outcomes from the Australian National Joint Replacement Registry, we will look at mortality and fixation around the world, then I will explain to you how we cement differently in a hip fracture to a primary total hip.

    If we start with the guidelines, it is of note that the American Academy of Orthopaedic Surgeons actually strongly recommend the use of cemented fixation in elderly hip fractures and that is becoming an internationally recognised guideline.  There is no national guideline anywhere in the world that does not support the use of cement with a stem in a hip fracture.

    In the United Kingdom, the NICE guidelines have long been held as a gold standard and they have very clear guidelines about how you should manage a hip fracture patient.  You want them to be in the theatre the day of admission or the next day.  You should have a dedicated list, you should have daily orthogeriatric input, the patient should be mobilising fully weightbearing the day of or the day after surgery and your hip fracture unit should take care of the patient through the whole journey.

    The guidelines recommend using a proven femoral stem rather than an Austin-Moore or a Thompson’s and you must use a cemented implant in patients undergoing surgery with arthroplasty and it is of note in the United Kingdom if you do not use cement on the femoral side the hospital does not get paid.  The guidelines are that strict.

    The decision on when to perform a total hip replacement is still not clear but increasingly it appears that people who are previously independent out of doors, using no more than a stick and are not cognitively impaired that a total hip replacement is a better option than a hemiarthroplasty.

    What do the results show:  The results show that a bipolar implant does better than a unipolar or a unipolar modular if you are going to treat with the hemiarthroplasty.  The difference is not great in the elderly but in the young it is very clear that you should use some form of cemented bipolar implant rather than a monoblock implant and these differences become even more dramatic with age and so the patients under 85 should probably have a bipolar rather than a unipolar and that is becoming increasingly recognised and we have seen in Australia that the use of unipolar implants is pretty well falling by the by.

    The question then is how do you fix the bipolar implant and the differences are incredibly dramatic when you start to look elderly patients receiving cemented versus uncemented implants.

    At 2 years there is a 2% revision rate for cemented stems and that is around a 6% revision rate for an uncemented implant. 4% might not sound like a big difference but it is actually 3 times the difference and that is 4 in 100 patients who will need another operation if you elect to go with an uncemented implant.

    The same is true with cemented hip replacements.  The evidence is increasingly clear that the cementless total hip replacements do significantly worse than the hybrid or the cemented and over 80 we probably should be using cement on both the acetabular and the femoral side.

    Recently, publications from the United States have come in and supported this and a large registry analysis written by Brian Springer et al actually found that there is a very high incidence of periprosthetic fracture when you use an uncemented implant and we are just starting to see the beginning of a trend and a big swing in the United States towards cementing stems in hip fractures in the elderly.

    In Australia in hip fractures 4% of stems are uncemented.  In the United States 93% of stems are cementless.  We have done some economic modelling and if we actually changed to doing what we do in Australia they would save their healthcare system many billions of dollars overnight and they would save countless lives.  Fortunately we are starting to see this change coming into play.

    The data as I said is starting to come out of the United States and there is a paper in JAMA from this year 2020 looking at just over 12,000 fractured neck of femurs.  Pretty much 50/50 cemented and uncemented and the one year revision rate for cemented was 1.3 and for cementless was 3.0 and if you do the Maths on the number of hip fractures treated in the United States that is an excess of 25,500 revision per year in the United States based on the decision to not use cemented total hip replacements and that is becoming increasingly unacceptable and difficult to defend.  In this study there was no difference in mortality at any stage.

    So you should use a bipolar in younger patients if you are going to use a hemiarthroplasty, cement in everybody, use a good quality stem and the role of total hip is becoming a little bit clearer but still not fully defined.

    So the debate is kind of lost on fixation, the uncemented people cannot defend the use of their implants with the Registry results.  So what has happened they have tried to bring in this lateral argument about mortality and created this myth that cement is not safe.  In the next few minutes we are going to actually address that issue and bust that myth.

    So bone cement implant syndrome is a rare yet devastating condition.  You see systemic hypertension, hypoxia, pulmonary hypertension, cardiac arrhythmias, and very occasionally cardiac arrest and death.  That probably occurs in a number of patients on the table even up to 20% in its mildest forms but it happens in uncemented and cemented probably in quite equal numbers.

    We published way back in 2011 on 25,500 hemiarthroplasties from the Australia Hip Registry.  We showed a slightly increased mortality on day 1 when you use a cemented implant, this had reversed by one week and persisted at month and by one year you were 50% more likely to have died if you have had a cementless than a cemented stem.  That is 20.7% versus 29.6%.  So if you were choosing a cementless stem you are killing 10 in 100 patients based on that data.

    In Finland they looked at 25,000 patients, similar numbers in 2014.  They actually found no difference in mortality at one week or one year but importantly cement was not implicated in increased mortality and like every other study they showed increased mechanical complications, femoral fractures and re-operations in a cementless group.

    Another study more recently in 2019 in Finland, 10,500 patients single institution, no differences in morality between fixation groups.  All the complications were related to medical code morbidities and not bone cement implantation syndrome.

    In Canada, again 2020, they showed increased mortality with the use of cementless fixation for fractured neck of femur.  In fact their number almost completely mirrored our Registry number.  At smaller numbers just around 6,000 no difference in mortality at 0,1 or 7 days and again at 1 year there was 10% lower mortality in the cemented group  So again they showed you are killing 10 in 100 patients by a year if you choose an uncemented stem.

    So if we look at the evidence around cement it is actually safe.  It is actually protective against mortality in nearly every study and in no study that has been properly matched with patient characteristics does cement does cause an increased risk of mortality.

    You may very rarely see a bone cement implant syndrome but if you are aware of it and I will show you in the next few minutes what we do to prevent this complication.

    So how do we cement in a hip?  What do we do differently?  And I would strongly recommend a paper written by Griffith Sedel, it was written in the Journal of Anaesthesia in 2015.  It was a collaboration between the British Orthopaedic Association, The Anaesthetic Society and the Geriatric Society of the United Kingdome and they made recommendations for the surgeons and the anaesthetist.

    When we approach the femoral canal, the first thing we should do is put a sucker down the canal and lavage aggressively.  We want to really wash out all the fat and all the debris because that is the material that gets embolised into the blood and causes the reaction.  When you are going to cement you tell the anaesthetist and the anaesthetist will draw up a vasopressor, that will bring the blood pressure back up.  In a primary hip we do not high blood pressure, in a fracture we want the blood pressure quite close to what it was pre-operatively.  We then put our cement in very late.  Again we are not trying to get a 25 year hip here, we are trying to get a patient alive and mobile and so if you put the cement in late there is much less residual monomer which means there is much less likelihood of bone cement implantation syndrome.  You then put your stem in early and slowly so you do not see that big push of debris into the circulation.

    The anaesthetist has a role, they have to keep the patient well hydrated and they have to maintain the blood pressure and as I said they have to have a vasopressor in a syringe ready to go if anything happens when you are cementing.

    You do not need the perfect x-ray. A white out is probably a bad thing in a hip fracture, it is okay to see a radiolucent line, it is okay to not have the perfect cement mantle, it is much more important to have a mobile live patient who is going to go on and have another 10 or 15 years of quality life.

    So what is the standard of care in fractures?

    • Position input
    • Early surgery
    • Appropriate surgical and anaesthetic technique
    • Cement every single femoral component and avoid monoblock stems in younger patients

    If you meet the standards of care we are going to see a significant increase in the survivorship for both revision and mortality and I thank you very much for your attention.

    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.