Friday, November 27, 2015

DVT and Thee

by Bob Albright, D.O.

The topic for this month's column is deep venous thrombosis (DVT), an extremely dangerous condition where a clot forms in the largest of the venous vessels of the upper and/or lower extremities. This condition results in sudden swelling of the affected limb, often with associated warmth, redness of the skin and a deep aching pain. DVTs can masquerade as muscular or myofascial trauma and skin infection, also known as cellulitis when extreme.

The truly life-threatening issue arises when the clot breaks loose (embolizes), traveling up to and through the right side of the heart and lodging in the pulmonary circulation, thus obstructing the blood flow leading to the lungs. This condition results in large sections of the lung being unavailable to exchange carbon dioxide and oxygenate the blood. Critically low oxygen levels result, usually associated with chest pain. This condition is known as a pulmonary embolus (PE). Unfortunately, the symptoms of this condition are often sufficiently vague and relatively mild to those of us “used to” being uncomfortably breathless that often athletes specifically seek care late.

While no definitive studies on incidence or prevalence of DVT or PE exist specifically for long-course triathletes, many scholarly works report the relatively high risk endurance athletes may face with respect to the general population.

Why do these clots happen?
Doctors are taught to think of Virchow’s Triad in settings of abnormal clotting situations, I believe this was named for DR Triad, but I’m not sure…(!)

The following make up the triad of risk for clotting:

  • Stasis of blood flow (slow blood flow)
  • Endothelial damage (damage to the metabolically active cellular lining of the vessels)
  • Hypercoagulability (abnormal tendency towards clotting)

Endurance athletes often pride themselves on their low blood pressure and outrageously low resting heart rates. Coupling this tendency with post event inactivity, often forced due to travel or injury, add in low intravascular volume/dehydration and we are all set up for risk number one.

Endothelial damage due to direct trauma of the vessels, perhaps from the saddle; a crash, fall or thrashing during the swim is very common. Arguably, the muscular trauma and breakdown, and free radical generation of prolonged exertion may lead to direct activation of the endothelium. This damage incites the clotting cascade, which will hopefully fulfill only its function of preventing bleeding -- but may become exuberant and lead to clot formation. This explanation has been used among athletes without other direct risks for clots.

Hypercoagulable states may be inherited or developed during our lives. There are many well-known clotting tendencies due to abnormalities in our body’s clotting-declotting mechanisms. These can be detected by a standard panel of blood tests. Clotting tendencies can also be caused by certain medications. Chief among these are hormones. Oral contraceptives, certain estrogen/progesterone compounds and erythrocyte stimulating agents have all been implicated. What the heck is an erythrocyte stimulator? EPO my friends, also known in other guises as procrit, aranesp, epogen and most recently cera. These banned substances increase the number of red blood cells raising the hemoglobin and hemotocrit levels to the point where the blood sludges, and clots. Several tragic deaths in the athletic world may be directly traced to use/abuse of these agents. Testosterone and growth hormone have also been implicated as causing DVTs and PEs. Other situations of aquired clotting tendencies include smoking, certain kidney problems, and even cancer, but, most importantly, dehydration (low effective circulating volume) iis a very common theme among athletes with DVT/PE.

How is a DVT diagnosed?
First of all get to your provider ASAP! The standard ultrasound will reveal the clot, as long as it hasn’t moved!

A PE can be difficult to diagnose. Most agree that a Computed Tomography (CT) scan with intravenous dye is the most effective evaluation. There are other methodologies however, even including a transfemoral pulmonary angiogram, which are effective as well. These are most often hospital-based tests.

How is a PE or DVT treated?
The primary goal is to prevent the clot from enlarging or, in the case of a DVT, prevention of embolization. Preventing further clotting requires medications which interrupt the clotting cascade.
Heparin products (IV or Sub q) and/ or vitamin K antagonists (Coumadin-oral) are utilized. These agents obviously render a patient vulnerable to bleeding, and this must be monitored very closely.

Clot dissolving agents such as TPA or streptokinase are controversial and are only used in life-threatening cases of PE due to their high hemorrhagic (bleeding) risks.

A filter in the vena cave, the major blood vessel leading from the lower extremities to the heart may have utility when blood thinners or lytic agents cannot be used due to recent surgery or ongoing bleeding (say -- from an ulcer). Once a person is on therapy, it will be monitored for effectiveness. The risk of a clot moving is extremely low once effective therapy is underway. So, the period of inactivity can be minimal. However, the damage done to the lung may be severe enough to limit aerobic activity for an extended or even permanent time frame. Do not underestimate this situation, PEs can be fatal.

As with most, if not all medical issues, it’s best to prevent this catastrophe.

So, how NOT to get a CLOT:

  1. Stay well hydrated -- urine needs to be pale yellow at the darkest
  2. Move, every two hours at least, and if you can’t get up and around, do the alphabet with your big toes on both feet, stretch, move your arms
  3. Use compression garments -- knee high is enough
  4. Elevate the legs
  5. No EPO, growth hormone or testosterone -- you just might die.
  6. No smoking, which is not a major issue among athletes, granted.
  7. If you are injured or immobilized, particularly after a major athletic effort, ask your provider if you could safely take an 81 mg Aspirin daily, or even sub q heparin.

Many excellent resources are available online -- but feel free to e-mail me with any other questions.

Bob Albright, D.O., is a Nephrologist and Assistant Professor of Medicine at the Mayo Clinic in Rochester, Minn. You can contact him at

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