Great question, thanks for bringing this up! I guess, patients have to be stratified by thromboembolic risk before making decision. In cancer patients for example, it will be better to keep the chemical prophylaxis going and do compression/ice. For patients with less risk for DVT, I believe stopping is the way to go. I don't think there is enough evidence to support any of the available agents having less bleeding complications.

Thank you, Dr. Piponov, for your post. I think my opinion coincides with yours. Anyway, in some cases we have to choose the lesser evil. The problem is that we hardly predict which is the lesser evil. 

Regards 

The common prophylactic dose of 40mg Clexane does not usually create haematoma problems (this does not apply to other agents as warfarin or rivaroxaban which are prone to create haematomas).

In case of such clinical symptomatology (presentation of haematoma) following prophylactic dose, there is potentially the indication that there are some additional factors helping this creation. Usually are these that influence the Liver function and possibly are due to the influence of other medication (usually) or condition of the patient that was difficult to detect prior to surgery with the routine blood tests,

If vascular injury is eliminated (this is very rare complication) my preferred treatment will be:

Compression bandage (if necessary and feasible)

Stop anticoagulation

Check INR and liver function

Observation and in rare cases (if indicated) Fresh Frozen Plasma

In the last 2 decades there was an aggressive introduction of chemical prophylaxis of DVT for major orthopaedic surgery (THA,TKA,etc.) supported by a number of "firma-oriented" consensus documents. This sort of anti-coagulation became "mandatory" for joint replacement, and I think it is done without proper selection of the DVT-at risk-patients. A fear for  judicial problems is present among surgeons.

On the other hand, it is generally acknowledged that anticoagulants (Warfarin, LMWH, etc.) are among the potential causes of wound haematomas and wound drainage with a serious risk of deep infection.

In my practice I  stop or reduce the dosage of anticoagulants if a persistent  wound drainage continues after 48-72 hours postoperatively unless these patients belong to the group of high risk for thromboembolic complications.  

Anticoagulation for VTE (as it is called now) as you say is "mandatory" treatment to treat mainly lawyers than patients. Orthopaedic surgeons are sceptical all the time about this treatment. On the other hand other medical disciplines say that this scepticism is not founded as VTE is presented and admitted under Medicine and not Orthopaedics so the Orthopaedic data is wrong.

All started with a report of abdominal surgery that resulted to fatal PE and since then as all surgeries have the risk of fatal PEs the "treatment" applied. Because we live in an evidence based time, it was necessary to create "evidence". As the medications were expensive the companies provided them and this way they controlled the published results.

The agents used are variable and they have complications that may result to expensive treatments. NICE produced guidelines that are disputed by the Orthopaedic surgeons and because of this they created amendments. A lot of surgeons still are using aspirin. Still there is no definitive solution to the problem and all treatments are disputed.  Despite that "anticoagulation protocols" exist. It is found that LMWH has the fewer complications in a prophylactic dose.

I agree with you as I have mentioned to stop completely and monitor the patient and pray not to develop any infection in the area. I do not use any more drains so only the clinical picture and the swelling is showing the risk.

I agree with you, George. Unfortunately,  the chemical antithrombotic prophylaxis as practiced today represents a "dead" lock which is difficult to overcome. To pray not to develop any wound infection or to pray (I would add) not to meet the patient's family lawyer seems reasonable. But this is not a medical solution.

I remember a classic paper by Warwick et al. where they reported 0.3% mortality rate from fatal PE after hip joint replacement independently on the prophylaxis done or not done. They  also said that a RCT proving the benefits of chemical prophylaxis should include at least 26 000 cases divided randomly in the two groups. It was absolutely right for the small percentage of fatal PE incidence.  This rate was regularly confirmed by my experience in my clinic (in my active years) where we have had around 1500 THA and TKA per year, and unfortunately - 4-5 patients with exitus lethalis from PE. 

The Xa inhibitors give some hope for less wound complications, but high-quality RCT's on their effects on surgical haematomas rate and wound drainage are yet not present. However, I wonder if this medication line is not a new "firma-oriented" wave.

Dear Panayot,

I am old enough to remember the days without the "routine" anticoagulation and I must say that during that time I had not witnessed any PE, fatal or not. Possibly the swollen calf now and then (do not forget that at that time a total joint was staying in Hospital between 15-21 days) which was settling down with more bed rest and gentle supportive in bed mobility. Since the anticoagulation started I had seen PE almost every few months (minor but symptomatic, thank God no fatal) and from all these years of practice three of my patients received long term or even life long anticoagulation. My humble opinion is that small thrombi formed in the lower leg veins before the anticoagulation were giving local symptoms and they were resolving over time, but now they are mobilised due to the circulation of the drugs and they ultimately reach the lungs. This is an anecdotal "evidence".

You are mentioning of new research. I believe that all pharmaceutical research is, as nicely you point out, "firma-oriented". They are providing the money. It is the same as the papers which are written about new prosthetics without any clear follow up. Up to now there is no clear independent paper supporting the one or the other medication.

We are trapped in this "treatment".

Dear George, 

I think we are  about the same age. I began my practice as a resident in orthopaedic surgery in 1973. So I am a witness of all that you are writing about prolonged bed rest and late ambulation of THA patients in those times, as well as that controversial   metamorphosis of antithrombotic prophylaxis from none to routinely applied different agents and dosage. Furthermore, I share entirely your opinion for the possible mobilization of thrombi through the action of anticoagulants. At least this hypothesis is not rejected by now. 

Presently, there is a new controversial combination of anticoagulants with tranexamic acid (antifibrinolytic). In any case, there is an avalanche of papers that find this combination very effective in an attempt to reduce bleeding after joint replacement without increasing the rate of thromboembolic complications. This is really very interesting.Unfortunately, I do not have personal experience and have to rely upon literature. 

Dear Panayot,

I have used tranexamic acid and in my opinion has some failts. I have noticed Dyspnoea post op and the Radiological investigations show mild PE in some cases. This usually is given at induction but now I changed and for the TKRs I give it after the tourniquet is released. Discussing with colleagues we fear about inducing PEs and we think to abandon the idea of administer it. We had within six months about five or six patients with mild PE  (out of all operated patients 25 per week) On top of that we give anticoagulation for 6 weeks. This is a vicious circle. 

Really, this combination is not logic. 

Regards

This was discussed also with the haematologist who agreed. Tranexamic acid to stop bleeding at the immediate post op period and anticoagulation for six weeks as prevention to VTE.

If the patient is not a high risk for PE then logically the LMWH must be stopped and the treatment of haematoma should take the priority

There are some data that most of the thrombi start their formation the first 24-48 hours after major injury or major surgery as a response to trauma. So this period seems to be critical for an effective antithrombotic prophylaxis. Giving tranexamic acid during operation or at the immediate postoperative period seems to block the fibrinolysis and enhance the formation of thrombi. This is logic, isn't it ? 

no embolism can kill;  compression dressing is enough and if  hematoma :  possible evacuation 

• Wound complications - especially bleeding complications are 'in your face' issues while the DVT is a perceived threat. Not to counter bleeding and persisting with LMWH is counterintuitive is just wrong.
• DVT prophylaxis can be continued with mechanical means
• DVT chemical prophylaxis is industry driven and more from fear of legal issues , perhaps that's is obstructing clear thoughts