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Forum Name: Hematology Topics
Question: Abnormal Clotting Unknown Disorder
|Trenna - Wed Jul 28, 2010 4:33 am||
I am speaking not on my behalf but the poa of a dear friend has asked me to consult with any and all professionals I can contact, I've already reached out to my local peers and have found no help.
My friend, we'll call her Norma, is 46yrs old. 3 pregnancies, 3 live births. No history of substance abuse, alcohol or drug related or otherwise. African American, with a pneumonectomy a year ago to her R full lobe.
She has been experiencing mild to major clots forming in her legs, the embolisms never reach levels where surgery has been required. She's been able to take medications to dissolve any resulting clots, but the severity and regularity of these clots are continuing though she regularly takes anti-clotting medications, ie coumadin. This has continued for 13 years. She can't work because if she did any physically exerting labor a clot could break off and possibly result in death. Of course we are all worried.
Last night she was hospitalized, yet again, with what we believe to be a clot. Her symptoms were angina, trouble breathing, dizzyness, headache, and fever.
We are VERY worried about her. Please help.
|Dr.M.Aroon kamath - Fri Jul 30, 2010 9:38 am||
I certainly share your concern for Ms.Norma.I will try to provide you a bit of background information which may be of some help to you.
Pulmonary embolism is generally classified into 3 major clinical types.
- submassive and
Thrombophilia(an incresed tendency of blood to clot) is usually categorized into two types,
- acquired and
In acquired thrombophilia the abnormal clotting is usually related to a specific cause, such as prolonged periods of bed rest after surgery, trauma to the leg, or a malignancy.
In inherited thrombophilias, there is a tendency to form clots due to a genetic predisposition (inherited).
The inherited causes are AT-III deficiency, protein C and protein S deficiencies, dysfibrinogenemia, and activated protein C (APC ) resistance. Most individuals with APC resistance have a mutant factor V molecule (factor V Leiden) - named after a city called Leiden in the Netherlands where it was first identified in a family. Another mutation, the Prothrombin G20210A mutation is also frequently co-inherited in Factor V Leiden carriers. This is in fact the second most common genetic defect for inherited thrombosis, with Factor V Leiden being the most common.
About 5% of Caucasians have factor V Leiden, and it is more common in individuals of European ancestry. In the US, approximately 1-2% of African Americans, Hispanic Americans and Native Americans also have the mutation. Factor V Leiden is rarely found in Asians.
Any person who is homozygous (that is, he or she inherits a mutation in both copies of their gene, one from each parent) they are at a greater risk to develop a blood clot than an individual who is heterozygous for the mutant gene.
The risk also multiplies if they have both factor V Leiden and prothrombin G20210A.
The clinical course of most patients with pulmonary embolism is one of gradual resolution with re-establishment of flow in the pulmonary arteries. A small group of patients, experience recurrent showers of emboli which may ultimately occlude a large part of the pulmonary small vessel bed with development of chronic “vascular” type of pulmonary hypertension, which may even be fatal. Whether anticoagulation is effective in the treatment of recurrent thromboemboli is undetermined.
Recurring embolic episodes while on anticoagulation is an indication for inferior venacaval filters. Ms Norma, as you have indicated, has had a pneumonectomy(indication?). As she has only one functioning lung presently, it is unaffordable to lose any of her remaining lung reserve. Thus, there seems to be an absolutely strong indication for placement of an inferior venacaval filter.
As she is presently admitted to a hospital, I am certain, the treating doctors will consider all options.
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