Deep Venous Thrombosis (DVT)  remains a significant concern in TJA because it can lead to Pulmonary Embolism, one of the few life-threatening complications after TJA (its the 2nd cause of mortality following cardiac events) [128] [129]. All patients undergoing TJA are deemed “High-Risk” for VTE complication, although patient risk factors allow for further stratification of risk of VTE.  

Incidence of DVT.  There is a significant difference between the rate of overall DVT versus the rate of symptomatic DVT.  A recent Japanese study examined VTE rates at Postop Day 10 via doppler of all TJA patients and found a significant discrepancy between rates of overall and symptomatic VTE in both THA and TKA [124].  In THA, overall vs. symptomatic DVT 12.6% vs. 0.2%.  In TKA overall vs. symptomatic was 24.3% vs. 0.9%.   A similar study from Europe also identified a large difference DVT [130].  Older studies using venograms to evaluate for DVT similarly found overall DVT rates between 20 – 60%, with over 50% occurring in calf veins.  In general, the overall rate of VTE varies widely (often reported around 20 - 40%, despite DVT prophylaxis), while the rate of symptomatic VTE is roughly 5% (ranges between 1 – 10%). PE occurs in 1-2% of patients, and fatal PE occurs in about 1 in 1,000 cases (0.1%).

 Thromboprophylaxis has dramatically reduced the incidence of VTE.  In patients receiving no VTE prophylaxis, the overall rate of VTE varies from 40 – 60% [133] [134] [135], significantly higher than the aforementioned rates in patients treated with prophylaxis. The overall rate of PE in patients without anticoagulation is 0.5-2.0% PE and 0.1-0.5% fatal PE.  

Health care management studies, looking at VTE rates beyond TJA procedures, have also found this large disparity between symptomatic and silent DVT, and remark “the more you look, the more you find”...reflecting a correlation between aggressive VTE monitoring (using Doppler surveillance) and higher VTE rates [131], similar to the "Observer Effect" - the measurement of a system cannot be made without affecting the system.  

As a result, while advances in doppler technology and compression protocols have improved DVT detection to reliably replicate gold standard invasive vascular studies [132], AAOS, AAHKS and ACCP guidelines discourage the routine use of Doppler screening in all TJA patients because the significance of DVT, particularly in the asymptomatic patient, is unclear.  The true incidence of VTE is high, yet because a large percentage are clinically silent (between 50-80%), the rate of clinically significant VTE is very low.  

TKA is generally associated with a higher rate of overall and symptomatic DVT.  It is also possible that the use of tourniquets in TKA increase hypercoaguability and are thus partially responsible for increased rates. Its also possible that normal postoperative symptoms in TKA (such as lower leg swelling, bruising, and pain) are mistaken for DVT symptoms, leading to higher rates of DVT screening and thus higher rates of “symptomatic DVT”.  

Timing of VTE.  When does VTE occur in the postoperative period?  This is also debatable.  While many argue the thrombotic event occurs soon after surgery (when the pro-coagulation pathway), other data suggests that it occurs a few days after surgery. 

Januel et al. reported symptomatic VTE rate of 0.53% in THA and 1.09% in TKA while patients were hospitalized postop [136].   Risk of PE was 0.14 to 0.27%. Other studies have found slightly higher rates of PE with 0.6% in THA and 1.47% in TKA during the hospital course [137]. Parvizi et al reported that 80% of PE occurred within 3 days of index surgery [138].  Yet other reports suggest 70% of VTE is diagnosed after hospital discharge. A study of 5,000 patients found the average DVT in THA occurred at 21 days, and PE at 34 days, while the average TKA DVT occurred at 20 days, and PE at 12 days [133].  The variability between studies highlights the general challenge in identifying clinically significant VTE.


AAOS, AAHKS do not provide treatment recommendations.  ACCP does provide treatment recommendations.  The challenge is that much of the data on VTE treatment, and risk of DVT progression, is not specific to TJA, but rather extrapolated from studies on other surgeries.  It is therefore unclear how these recommendations translate to TJA cases. Orthopedic surgeons must weigh the benefits of treatment with the known risks of bleeding that comes with prolonged anticoagulation of a postop patient.  The ACCP treatment recommendations do not appear to balance this risk/benefit ratio as they are not speaking specifically to TJA cases.

How do we know which DVTs are significant and which need to be treated? Do we treat all DVTs the same? It is challenging to reconcile the large disparity in numbers: 20-40% overall DVT (high prevalence) and 5% symptomatic DVT (moderate prevalence), 1% PE (low prevalence) and 0.1% fatal PE (very low prevalence).  

Do we care about DVTs themselves, or do we really only care about DVTs because of their risk of becoming a PE?  Are DVTs accurate markers for patients at risk for PE? The risk, the actual number of DVTs that propagate to PE is incompletely understood.  DVTs are not created equally.  A large above-knee DVT is different than a small calf vein DVT.

Lotke et al. used venograms and V/Q scans to correlate the relationship between DVT and PE [164].  They found, similar to other studies, that despite DVT prophylaxis, a high incidence of infrapopliteal DVT (IDVT), nearly 50% of patients [165].  These thrombi were 2.5x more common in TKA, yet the overall rate of PE was the same in THA and TKA.  These findings suggest a low correlation between IDVT and PE risk. It suggests that IDVT are not clinically significant. In contrast, there was a significant correlation between Popliteal/Femoral Vein DVT and PE, likely due to the larger caliber of these veins and thus larger sized clots.  Larger clots are more prone to propagate.

Yet the picture is not so clear for these isolated calf DVTs. Haas et al. studied over 1000 TKA patients with venography and V/Q scans, found a similar rate of 50% calf DVT, and found a significantly greater risk of symptomatic and overall PE in patients with calf DVT compared to patients without clot. Of the 655 patients with calf DVT, 11 (1.7%) had symptomatic PE, while only 1 (0.2%) of 498 patients without clot presented with a symptomatic PE [166]. Thus the treatment of calf DVTs remains controversial.

If the goal of VTE treatment is prevent the devastating complication of a symptomatic PE, is DVT even the best marker for PE risk? Other studies have demonstrated that cancer, congestive heart failure, and thrombophilia disorders have a much higher correlation with PE risk, with PE occurring in up to 10 – 30% of cases [129]. Parvizi et al reported on >26,000 TJA cases and found 1.1% risk PE with 0.2% fatal PE.  Risk factors for PE include obesity, higher Charlson Comorbidity Index, presence of DVT, TKA (vs. THA), COPD, and depression [167]. Bohl et al. found similar risk factors[168]. Thus DVT appears to be one of many risk factors.  It appears that there are many factors that influence how to treat a DVT.

Returning to the ACCP guidelines, VTE treatment recommendations are:

2.3.3. In patients with acute isolated distal DVT of the leg who are managed with initial anti- coagulation, we recommend using the same approach as for patients with acute proximal DVT (Grade 1B).

They do not distinguish between size or location of the clot.  The emphasis is on the fact that any patient being anticoagulated, that still presents with a clot, should be considered at higher risk for propagation.  Again however, this does not appear to be specific to orthopedic/TJA patients.


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