Perhaps someone will investigate Serena's diet.  We all need to "speak out" against the pro-inflammatory and prothrombotic nature of the food that most Americans eat!!!

In adittion to the fact that she probably could have been taking hormonal pills, it could also be possible that the origin of her pulmonary embolism be localized in a highly demanded arm (Paget-Schroetter syndrome).

 Miss Serena es portadora de problema  heredo genético de hemostasia, (PAI-1,Proteina S-C, heterocigota u homocigota para protrombina etc.)

Dr.Alberto More

Dear Dr. More:

Would you please clarify your comment?  Are you speculating that she is a carrier of a hypercoagulability marker or is this something you know as a medical fact?  To me, the most important point is that at age 29, an internationally recognized superathlete suffered acute pulmonary embolism.  We need to raise  awareness of PE among clinicians and the public.--SZG

A thrombophilic workup is clearly in order here.In such a young a potentially fertile woman as this;contraceptive meds(birth control pills) are a serious causative factor.

A thrombophilia workup might help satisfy intellectual curiosity but won't necessarily guide management regarding the optimal duration of anticoagulation.  Serena had no recent (within 3 months) surgery or trauma.  If she's not taking birth control pills, the odds are high that she suffered idiopathic and unprovoked PE.  And if this is the case, her risk of recurrence is high after discontinuing warfarin, regardless of the workup for hypercoagulability.--SZG

to Goldhaber; beyond 'Ifs & maybes'".A diagnostic evaluation(thrombophilia workup) to determine the causative factor if possible is appropriate in this case, regardldless of the length of anticoagulant treatment warranted following that evaluation.Such a workup may very well have significance beyond possible recurrence; i.e pregnancy and adverse reaction to certain anticoagulants.--JS

Understanding the cause of her thromboembolic episode is not merely an academic exercise. If she chooses to become pregnant in the future or have kids, the cause of her event is important to understand to provide more appropriate management during pregnancy and risk for her future children as well (not to mention post surgical management in the future). If it was due to antiphospholipid antibodies versus Factor V Leiden mutation for example would have different implications for her children.

 excellent points! And I agree with you,150%!!!!!!!

avoid coumadin use fragmin or equivalent long term and for travel. Less risk of bleeding and quicker reversal easier to manage.

I agree with Dr Goldhaber. The most important risk for thrombotic events during pregnancy is a history of VTE. For example, in the case of factor V Leiden mutation, a prior history of VTE increases the likehood of VTE during pregnancy from 0.2 to 10%. In other words, irrespective of the presence of a inherited thrombophilia, this patient has a high risk of VTE during pregnancy if the actual event is unprovoked.

I have seen athletes stricken by VTE from two sources: axillosubclavian thrombosis from the axillosubclavian complex and May-Thurner from the iliofemoral venous complex. Generally, these have been healthy individuals and they frequently have been found to have an underlying thrombophilia. Many have had these mechanical issues without reporting pre-existing symptoms. The mechanical issues and underlying thrombophilias have generally been superimposed on another feature such as flu-syndrome, trauma, air travel, initiation of OCPs, etc. which finally tripped the scales in favor of thrombosis. In Serena's case, where did the VTE originate? I am more interested in how she was evaluated and treated than I am in the PE itself. A psotphlebitic extremity in her case would be disastrous as well.

Do we really know what risk factors may have been temporally related to this PE?  I read that the cut that led to surgery was back in July; but I also thought that I'd read that she had more than one surgery.  Also, in one AP report, a picture showed her sitting with her legs crossed at the knees while she had a hard lower leg cast on the leg that was on top of her knee.  Do we really know when the foot/leg problem completely resolved?  Might the PE have resulted from a provoked and unrecognized DVT that developed earlier?  If the cast was on her left leg (as I think it was), might she have had surgery + infection + immobilization + possible May Thurner syndrome all contributing to a provoked DVT that went untreated and led to the PE?

I can certainly attest to Dr.Goldhaber' expertise in this area.He certainly did a helluva job taking care of me.Almost 10 years now and no complications of any kind.Still working as a firefighter.Thank you again Dr.Goldhaber!

Dr. Goldhaber,

Thanks so much for doing this piece. The possible diagnosis of acute PE should be foremost in our minds regardless of age or gender for unexplained tachycardia, syncope, shortness of breath or unexplained RV dyfunction or dilitation by echo. I  tell my residents and students that we  can't just wait  for the classic pleuritc chest pain or unexplained hypoxemia. 

Excellent points and thanks so much!

Melissa

Something that probably will never be known and is pure speculation at this point is whether Ms Williams, as a world-class athlete, may have been using an erythropoiesis stimulating agent. The prescribing information for ESA's carries a black box warning for prothrombotic risks.

I read the headline of this blog and it has NOTHING to do with what is being discussed here. The injury was on the right foot so MTS is ruled out. We can NOT take the age, sex or physical shape of Serena in consideration because it does NOT apply, we ALL know that it does not work like it use to in the dark ages, at least I hope that all clinicians should know that.

Until any of you have any HARD FACTS, you are all guessing, and in some cases some clinicians still guess even with a patient right in front of them, yes I agree DVT, PE, UEDVT... are hard to diagnose and that is why so many cases are misdiagnosed.

So many risk factors are present:

-Air travel, we all know how much a tennis player travels during a season(yes those over four hour flight are the main ones)  and nobody knows if Serena knows to keep her calves active and keep herself hydrate(with water, not coffee nor alcohol) during a flight.

-Going from highly active to almost innactive for an athlete can be the cause, but again, it all depends on her awareness level towards DVT...If she is like MOST post DVT patients, I would suspect that  she was not aware of any of the precautions that have to be in EVERYBODY's face, more education , more awareness is what many post DVT patients are saying and doing.

-Is she on the pill??

-Was she on  steroids, like so many Tabloids would like to hear...

-Or is it genetic?

 So back to Serena Williams, Idiopathic (unprovoken) is the most common answers for athletes or people like myself who are not athletes but close...

So back to the guessing games, who is next at rolling the dice???

Thanks so much for your comments, Melissa.  These are precisely the take home points of this Clot Blog.  We have great blood screening tests and imaging tools to diagnose PE, but unless we think of this illness known as the Great Masquerader, we will continue to underdiagnose this potentially fatal condition.  Best regards, Sam

I am wondering if there will be further investigation into Serena's previous Pulmonary Embolism, now that her sister Venus has been diagnosed with Sjogren's? I am a 53 year old woman who was diagnosed 5 years ago with Sjogren's, Raynaud's and probable Scleroderma.  My mother also had Rheumatoid Arthritis and suffered many strokes due to a blood clotting disorder that she had in conjunction with her other auto immune problems.

Four years ago, I suffered a DVT and a Pulmonary Embolism although I was very active (First Grade Teacher) and had no other risk factors, except the auto-immune diagnosis and my genetic history (from my mother).  I was diagnosed with antiphospholipid syndrome and told that I would be on blood thinners for the rest of my life.  I have continued to have complications in my right leg from the DVT I suffered 4 years ago, as well as problems in my fingers and hands with Raynaud's and Scleroderma. I am wondering if since these problems occurred in two sisters, if any investigation has been made into the fact that they could be related.

Jeannette Gonzales

I've had antiphospholipid Syndrome (aka Hughes Syndrome) for some 30 odd years (before Prof Hughes research led to the condition  being named after him). Initially manifested as repeated pulmonary emboli. Been on warfarin for many years and will be on them for life. In last few years diagnosed with Srogrens Syndrome and yes, antiphospholipid sydrome and sjogrens combination  is not uncommon it seems.

There are two tests for antiphospholipid syndrome which, whilst not definitive, can be indicative