"If you prick us, do we not bleed?" The answer to this Shakespearean question is of course yes, but fortunately, not for long. We don't simply bleed our entire blood volume out each time we suffer a cut thanks to a complicated cascade of molecular and cellular processes that result in the formation of blood clots.
Under normal circumstances, whenever a blood vessel is compromised, platelets and coagulation factors are activated to plug the breach and bleeding ceases. Soon, the underlying damage to the vessel wall is repaired and the clot dissolves away.
This "clotting cascade" is under tight control. This is because while the formation of clots may be life-saving, in smaller arteries it causes significant disease. All of our cells are dependent to varying degrees on a continuous supply of oxygen.
The heart and brain are examples of organs that do not tolerate any interruption of this supply. Thus, a clot that blocks an artery in the heart results in a heart attack. One that occludes a vessel in the brain causes a stroke.
Clots may also occur in the veins, principally in the arms and legs. When this occurs, blood flow back to the heart may become impaired. More importantly, though, these clots may shear off and travel to the lung, a process called embolization.
Pulmonary, embolism (PE) is a serious medical problem and accounts for a sizable number of sudden deaths in North America. Fortunately, though, most PEs are minor, although they may be a harbinger of a more significant future PE and are therefore treated aggressively.
In the late 1800s, Dr. Rudolf Virchow identified the risks for the formation of deep vein clots (thrombi) and subsequent embolism. Virchow 's triad consists of vascular injury, hypercoagulability (increased ability to coagulate) and stasis (pooling of blood), and it remains the best means of identifying who is at risk for venous thromboembolic (VTE) disease.
Recently cases of athletes, including triathletes, with VTE have been reported in the medical literature. The actual incidence of VTE in this group is unknown, but it is easy to appreciate how each element of Virchow's triad can occur in a triathlete and predispose to VTE.
VASCULAR INJURY: Running long distances induces microtrauma to the veins of the legs. Normally this isn't significant nor does it cause any lingering effects.
HYPERCOAGULABILITY: Dehydration con- centrates platelets and coagulation factors in a smaller amount of blood volume. Once again, in isolation, this is not a serious issue during training or racing.
STASIS: lf, after sustaining microvascular trauma and becoming dehydrated, one then sits in a car or a plane for more than four hours, they %al have venous blood pooling in their legs and the third component of the triad will be in place.
What then can a triathlete do to lessen chances of developing VTE? Essentially, after any long distance race, it is important to rehydrate quickly and completely. If traveling, stay hydrated and try to get up and walk around once every two hours for five minutes or so. Finally, the use of compression stockings may help circulation, although the effectiveness of this treatment has not been conclusive.
Signs of VTE include calf pain and swelling or shortness of breath, chest pain and cough. These symptoms should prompt a visit to a physician who can perform the necessary tests to diagnose VTE.
Treatment consists of a three- to six-month course of blood thinners during which cycling is ill-advised, so it's best to work to prevent VTE rather than need to treat it.
V Jeffrey Sankoff, MD, is a two-time lronman triathlete and ER physician at the University of Colorado Healthy Sciences Center in Denver, Colo.
source: Triathlete_Sept2010
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