Here to educate is Kim Quinter, formerly the health/science/medical columnist from Flyers Faithful, who has graciously compiled the following detailed explanation of what has afflicted Flyers defenseman Kimmo Timonen for the second time in his Philadelphia tenure.
Kim is not a doctor, but she did stay at a Holiday Inn Express last night.
But seriously, Kim is graduate of James Madison University and currently works as a Physician Assistant at James River Family Practice in Newport News, VA.
Deep vein thrombosis and pulmonary
embolism. Fancy words, right? Do they sound scary? They should.
Thrombosis
is a blood clot and a deep vein thrombosis, or DVT, is a clot that forms in the
deep veins of the body. DVTs most commonly form in the lower leg, but they can
also form in other areas of the body, such as the groin and arms. When a piece of a
blood clot breaks off and travels through the blood, it is called an embolus. When
it travels to the lungs, it is called a pulmonary embolism, or PE.
DVTs can cause swelling in the extremity involved, can be in one leg or both legs, it can cause cramping pain, discoloration of the skin and warm of the skin. PEs will generally cause a sudden shortness of breath, sharp and stabbing chest pain, rapid heart rate and cough, sometimes with blood tinged mucus.
Blood is pumped out of the heart via arteries and returns to the heart through veins. Blood carries nutrients and most importantly, oxygen to all of the tissues and organs in the body. Blood comes back to the heart through big veins called the superior vena cava and the inferior vena cava and enters the top right chamber of the heart, right atrium. It is then pumped down to the then to the right ventricle (bottom chamber) and to the lungs to pick up oxygen that we breathe in.
Blood comes back to the heart from the lungs through the pulmonary veins to the left atrium, then to the left ventricle and then is pumped out to the rest of the body. When blood flow in the lungs is blocked, your blood does not become oxygenated, so the heart pumps faster to try to pick up much needed oxygen in the blood.
There are three things that are known to contribute to blood clots and the eponym given to these is Virchow’s Triad. It is comprised of hypercoagulability (sticky blood), injury or damage to the lining of blood vessels, and stasis (stopped) or turbulence of blood flow. When there are two of these three things present, there is medium risk for a blood clot; when all three are present, there is high risk for a blood clot.
A 21-year-old female college student smoker that flies to Europe for spring break would be considered medium risk for developing a clot. Smoking makes her blood sticky and sitting on a plane for 10-plus hours causes blood to sit in the legs or stasis of blood. If that same female had a heavy suitcase fall on her foot before boarding the plane, she would be high risk because now she has sticky blood, she will be sitting for the majority of a double-digit-hour flight because her foot hurts and she has had trauma or damage to blood vessels.
Specific risk factors for developing
a clot are:
- Prolonged bed rest
- Injury or surgery
- Pregnancy
- Birth control pills or hormone replacement therapy
- Being overweight/obese
- Smoking
- Cancer
- Heart failure
- Inflammatory bowel disease (Crohn’s disease and ulcerative colitis)
- Personal or family history of DVT or PE
- Age greater than 60
- Sitting for long periods (driving or flying)
- Inherited blood clotting disorders
I recall when Timonen was
first sidelined during the late stages of the 2008 playoffs with a small blood clot in his foot. At the time, I remember
thinking that he had trauma to his foot after blocking a shot and they were
flying, so it wasn’t completely impossible for him to have developed a blood clot. I hoped
it was a fluke occurrence and he wouldn’t have any other issues, however when
I heard recently that he had been diagnosed with a DVT and bilateral (both
lungs) PEs, I admit that I immediately imagined Timonen, one of my favorite players,
retiring this year.
Reports are that Timonen was diagnosed with a condition called protein C deficiency, which can predispose someone to developing blood clots. Protein C deficiency can be inherited (born with it) or it can be an acquired (caused by something else) problem. The normal human body has built in checks and balances so the things that make blood clot are balanced by things that will thin the blood.
When there is a thrombophilia (predisposition to clots) there is either too much of the clotting parts of the blood or there is too little of the thinning parts of the blood. Protein C is one of the natural blood thinners. One of the clotting factors, Factor V, is turned off, by activated protein C. In normal people, Factor V helps to activate an enzyme called thrombin, which helps to make fibrin, the meshwork that makes up a portion of the clot. In another type of thrombophilia, Factor V is mutated and cannot be turned off by activated protein C. This is called Factor V Leiden thrombophillia.
Reports are that Timonen was diagnosed with a condition called protein C deficiency, which can predispose someone to developing blood clots. Protein C deficiency can be inherited (born with it) or it can be an acquired (caused by something else) problem. The normal human body has built in checks and balances so the things that make blood clot are balanced by things that will thin the blood.
When there is a thrombophilia (predisposition to clots) there is either too much of the clotting parts of the blood or there is too little of the thinning parts of the blood. Protein C is one of the natural blood thinners. One of the clotting factors, Factor V, is turned off, by activated protein C. In normal people, Factor V helps to activate an enzyme called thrombin, which helps to make fibrin, the meshwork that makes up a portion of the clot. In another type of thrombophilia, Factor V is mutated and cannot be turned off by activated protein C. This is called Factor V Leiden thrombophillia.
Acquired protein C deficiency can be
caused by warfarin therapy (blood thinner to treat blood clots),
Protein C is decreased when there are new blood clots, so in a patient with several blood clots and suspicion for inherited protein C deficiency, protein C activity should be tested at a later time to determine whether there is a true, persistent protein C deficiency.
To treat DVTs and PEs, patients will receive anticoagulation (blood thinning) medications for 3-to-6 months. Anticoagulation medications are heparin, warfarin, low-molecular-weight heparin and newer anticoagulants, the direct thrombin inhibitors and selective Factor Xa inhibitors. Warfarin has been around for a long time. It works by blocking the synthesis of vitamin K dependent clotting factors (II, VII, IX, and X) and also blocks the two blood thinning proteins, protein C and protein S. Blood tests must be monitored closely while a patient is on warfarin and warfarin does not play nicely with many medications and foods, so diet must be very consistent while on warfarin therapy. It’s kind of a huge pain in the rear to be on warfarin therapy. The advantages of the newer anticoagulants is that they do not require routine monitoring and they play well with other drugs.
Fortunately, or unfortunately sometimes, anticoagulants do what they are supposed to do and they thin the blood. This typically is very troublesome when someone is bleeding. Warfarin is reversible by using vitamin K. The newer anticoagulants, though easy to take, have no antidote, so bleeding can be very difficult to control.
People that have had multiple thromboembolic episodes may need to be on long-term anticoagulation. This is not something to take lightly as there is risk of major bleeding which can be fatal. Another option for people with multiple thromboembolic events is an Inferior Vena Cava (IVC) filter. This is a small filter that is inserted through a blood vessel and placed in the IVC to prevent emboli from entering the heart.
Tomas Fleischmann, like Timonen, also had multiple thromboembolic events shortly after being acquired by the Colorado Avalanche. He has been anticoagulant therapy with a low molecular weight heparin that is injected every day. These injections are similar to insulin injections in that they are given into the abdomen or thigh. Fleischmann also wears a compression suit on plane flights now in order to keep blood circulating and help prevent clots and had surgery to have an IVC filter placed.
A high impact sport and anticoagulation therapy is not a good combination; every awkward crash into the boards, every bump, every hit on the ice would have the potential to be life threatening due to bleeding. Timonen and Fleischmann aren’t the only hockey players to have trouble with blood clots. Jed Ortmeyer, currently in the AHL, has dealt with several blood clots dating back to 2006. He has also had an IVC filter placed and is on lifetime, daily anticoagulant therapy. He times his medication so that it will be out of his system when playing hockey to reduce the risk of bleeding and also wears a compression suit while flying.
We will have to wait and see how Timonen and his team of doctors proceed with treatment. There is certainly precedent for Timonen to be able to return to play.
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