AWSOME WEBBLOG ABOUT AN ACTIVE YOUNG GUY WITH DVT

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You Can Dive With DVT and IVC - Incredible News from President of B|Braun

Incredible news for people who want to scuba dive with a vena cava filter (IVC) and for those divers taking high dosage coumadin instead of getting a vena cava filter (IVC) installed.

Divers, I have received an email from the president of B|Braun the manufacturer of the vena cava filter (IVC) that was installed to prevent a pulmonary embolism or stray blog clot from killing me. I was truly shocked to receive the email so quickly, I mean it was a long shot sending this email and I was desperate because I was going on trip to the Bahamas (Freeport, Pelican Bay). My doctor had told me that she would NOT sign off for the NAUI certification form. She called my vascular surgeon who told her she would be crazy to sign the waiver because the VC filter installed in me could not sustain the atmospheric pressure and it said so on the box.

This was untrue I learned. The president of the company emailed me and told me that the vena cava filter could withstand and atmospheric pressure after 8 months of being installed!

So for everyone who was told they could not dive because of a vena cava filter may want to check with the manufacture...

Basically there is a lot of miss information out there and doctors are either scared because of so many frivolous lawsuits or too busy to check the facts.

DVT and Pulmonary Embolism

Venous thromboembolic (VTE) disease, the syndrome in which blood clots form in the deep veins and often break loose to travel to the lungs, is one of the most difficult and serious problems in modern medicine. Early recognition and appropriate treatment of deep venous thrombosis (DVT) and pulmonary thromboembolism (PTE) can save many lives.

Problem: DVT causes morbidity and mortality both by its behavior in the deep veins and by embolization to the lungs and other parts of the circulation. Because DVT and pulmonary embolism (PE) are a single disease, it is misleading to consider the two conditions separately. Prospective studies in patients with proven DVT but without any signs or symptoms to suggest PE find that roughly half of these "asymptomatic" patients have experienced undiagnosed PE. The more precise the test, the more it appears that virtually every case of DVT embolizes to some extent. With or without PE, DVT itself may be occult. Two thirds of patients with proven PE have no DVT symptoms, and one third of the time it is impossible to find the original site of DVT without an autopsy.

All currently available diagnostic tests for DVT are more sensitive and more specific when a patient has lower extremity pain and swelling than when a patient has asymptomatic DVT. All are likely to miss thrombus below the knee or above the groin and are less sensitive for the detection of nonobstructing thrombus than for obstructing thrombus.

Frequency: The true prevalence of VTE in the population at large generally is underestimated because most studies depend on the recognition of clinically apparent disease. This approach fails for VTE because many cases are clinically inapparent and because many clinically apparent cases are misdiagnosed. The problem is compounded in retrospective studies, in which incomplete chart notes and inaccurate recollection further cloud clinical certainty.

The best epidemiological evidence today comes from the 30-year prospective study of men born in 1913. For every 100,000 person-years, this study found an incidence of 387 cases of recognized venous thrombosis, of which 285 subjects had a diagnosis of PE and 107 had fatal PE. This corresponds to an average of 39 cases and 11 deaths per year in a practice of 10,000 patients. One of every 9 persons develops recognized DVT when younger than 80 years, and clinically recognized VTE accounts for 1 of every 20 deaths in those older than 50 years. Autopsy studies demonstrate that approximately 80% of all cases of DVT and PE remain undiagnosed, even when they are the immediate cause of death. Therefore, the true prevalence in the population at large is probably much higher.

Although the prevalence of DVT and PE is highest in patients hospitalized and at bed rest with serious coexisting illnesses, the prevalence in ambulatory outpatients is not insignificant. Emergency department patients whose symptoms include pleuritic chest pain have a rate of PE of 21%.

Etiology: A clinical suspicion of DVT or PE often stimulates efforts to identify known risk factors for venous thrombosis. All recognized risk factors for DVT (and thus for PE) arise from the 3 underlying components of the Virchow triad: venous stasis, hypercoagulability, and vessel intimal injury. Although the presence of known risk factors increases the likelihood of PE, the opposite is not true because the absence of occult risk factors cannot be confirmed without an extensive workup.

The single most powerful risk marker for DVT is a prior history of VTE. In the absence of prophylaxis, patients who have had prior recognized PE or extensive DVT are virtually certain to develop recurrent VTE with surgery. An increased risk of DVT is also recognized in clinical settings such as the postoperative period, pregnancy, and the puerperium. DVT is common in patients with local trauma and stasis, such as that associated with a leg cast, and in those who smoke, are obese, or travel in confined circumstances (the so-called coach-class syndrome). Other clinical settings commonly reported as risk factors for venous thrombosis are reviewed here.

Anesthesia

Patients receiving general anesthesia have a 500% increased risk of DVT compared with patients receiving epidural anesthesia for the same surgical procedure.

Autoimmune disease and immune deficiency

Of patients with systemic lupus erythematosus, 9% develop spontaneous DVT. The lupus anticoagulant responsible for the excess risk is observed in persons with AIDS and in those with many other autoimmune diseases besides lupus and may be induced in healthy patients by phenothiazine drugs.

Blood surface antigens

Type A blood is associated with lower levels of antithrombin III and higher levels of factor VIII than type O blood. Women of reproductive age with type A blood are 4 times as likely to develop DVT compared with women with type O blood. This association of risk with blood type A does not extend to older men or to women past reproductive age.

Cancer

Malignancy is an important risk factor for DVT, and spontaneous DVT without an obvious cause is an important marker for possible occult malignancy. In 38% of cases of concomitant cancer and DVT, the DVT is detected first. The relative risk for cancer is 19 times higher for patients younger than 50 years who have had DVT than for those without a history of DVT. Fully 16% of patients with angiographically proven PE are diagnosed with cancer within 2 years.

Strokes and neurotrauma

DVT is common after stroke or neurological trauma. Without prophylaxis, half the patients develop acute DVT within 5 days following a stroke. Head trauma may cause defibrination, disseminated intravascular coagulation, and DVT. Forty percent of postoperative neurosurgical patients develop DVT. Stroke patients with a single paretic leg develop DVT in 60% of the paralyzed legs but in only 7% of the nonparalyzed ones.

Chemotherapy

Many types of chemotherapy increase the risk of DVT and PE. Some agents reduce the levels of circulating anticoagulants such as antithrombin III or protein C or S, some cause an increase in circulating procoagulants such as von Willebrand factor, and some depress fibrinolytic activity.

Coagulopathy

Deficiencies of protein C, protein S, or antithrombin III are well-recognized coagulopathies that together account for approximately 15% of the cases of DVT. Resistance to activated protein C accounts for many more. The lupus anticoagulant is another common coagulopathy that can be inherited or acquired.

Patients with familial deficiency of protein C or protein S often experience multiple episodes of DVT or PTE when younger than 35 years. Cancer, chemotherapy, vitamin K deficiency, oral anticoagulant use, surgery, and disseminated intravascular coagulation can trigger an acquired deficiency of protein C.

Antithrombin III deficiency may be familial or acquired. Most cases occur in patients with severe liver disease. If antithrombin III levels are reduced to half the normal circulating level, the patient is at high risk for venous thrombosis. More than half the persons with this deficiency experience PTE when younger than 50 years.

The most important coagulation abnormality remained completely unrecognized until 1995, when Ridker described a resistance to activated protein C that results from a single point mutation in factor V. This newly recognized hypercoagulable state, known as APC resistance or factor V Leiden, is present in 7% of the general population and is responsible for half the cases of DVT that were previously considered idiopathic. In current practice, any reference laboratory can perform the biological assay for APC resistance, and most can also perform the more accurate DNA test for factor V Leiden.

Fibrinolysis

Impaired fibrinolysis occurs in several inherited syndromes but is most common in postoperative patients, those taking synthetic estrogens of any type, and women who are pregnant or status postpartum.

Heart disease

Acute myocardial infarction and congestive heart failure increase the likelihood of DVT and PE, independent of bed rest or immobilization. Patients with acute myocardial infarction who are not receiving anticoagulation have a 26-38% rate of DVT, while similar patients treated for acute myocardial infarction but in whom infarction is eventually excluded have a much lower rate of DVT.

Hyperlipidemia

The presence of lipemic serum greatly increases the rapidity and extent of thrombus formation in response to vascular injury.

Immobility

Immobilization that produces stasis is the most important risk factor for DVT and PE. Hospitalized patients should be kept ambulatory whenever possible because DVT occurs in 10% of all patients placed at bed rest in a general medical ward and in 29% of those placed at bed rest in an intensive care unit. Unsuspected PE is a common contributing cause of death in all types of disease. Autopsy findings from patients dying in the hospital from any cause demonstrate PE in 15% of those dying after less than 1 week in the hospital and in 80% of those who die after more prolonged periods of immobilization.

Increasing age

Increasing age leads to an increased risk of DVT and PE, although whether this is entirely independent of associated factors such as other underlying illness and immobility remains unknown.

Inflammatory bowel disease

Patients with ulcerative colitis or Crohn disease are at increased risk for DVT and PE because of increased fibrinogen, factor VIII, and platelet activity and depressed levels of antithrombin III and alpha2-macroglobulin.

Miscellaneous

Homocystinuria and the Shwartzman reaction (ie, immunologic generalized thrombosis) both increase the risk of thromboembolism.

Obesity

Obesity (weight >20% above ideal weight) has long been accepted as a risk factor for DVT and PE, but the evidence supporting this association is not convincing. When associated factors such as history, illness, immobility, and age are taken into account, obesity may not truly be an independent risk factor.

Oral estrogens

No published prospective randomized studies have definitively tested and compared the prevalence of DVT or PE in patients taking or not taking oral contraceptives. Case-control and cohort studies based on clinical signs and symptoms of thrombosis suggest a relative risk of approximately 3-12 times higher for patients taking oral contraceptives compared with those not taking them.

Polycythemia and thrombocytosis

The risk of venous and arterial thrombosis increases linearly with an increasing hematocrit value. Forty percent of deaths in patients with polycythemia vera are related to thrombosis, but only a third of these are due to venous thrombosis. Thrombocytosis may increase or decrease the risk of thrombosis depending on the clinical setting, but platelet counts greater than 1 million most often reduce the likelihood of thrombosis and increase the likelihood of bleeding problems.

Pregnancy and puerperium

PE is the most common nontraumatic cause of maternal death in pregnancy, and the prevalence is even higher in the postpartum period. In Sweden, 53 peripartum maternal deaths occurred between 1971 and 1980, and 10 of these were due to PTE. Published reports of the incidence of DVT in postpartum patients ranges from 0.61-20 cases per 1000 peripartum months.

Prior DVT

Patients with a prior episode of DVT are 5 times more likely to develop new DVT compared with patients with no prior episodes of DVT. Prior DVT increases the risk of new postoperative DVT from 26% to 68%. A history of prior clinically apparent PE increases the risk of new postoperative DVT to nearly 100%.

Surgery

Perioperative DVT can result from minimal venous endothelial injury. The rate of postoperative DVT in patients who do not receive effective prophylaxis is 70% after nonelective hip surgery, 48% percent after elective orthopedic surgery, and 12% after elective general surgery. Approximately one fifth of the cases of postoperative DVT cause a clinically apparent PE, and approximately one third of these are fatal. Even when prophylactic heparin is used, 5-10% of postoperative orthopedic patients develop PE. Nearly half of all deaths in orthopedic surgery patients are due to PE.

Tissue antigens

HLA antigens Cw4, Cw5, and Cw6 are associated with an increased frequency of DVT and PE.

Pathophysiology: Millions of tiny injuries occur within normal blood vessels each day, and millions of tiny microthrombi are formed and lysed in a dynamic balance of functional hemostasis without clinically apparent venous or arterial thrombosis. The German pathologist Virchow demonstrated in 1846 that flow stasis, altered coagulability, or extensive vessel wall injury may cause microthrombi to propagate, resulting in macroscopic thrombi. Vessel wall endothelial damage is the most important of these 3 factors because even minor endothelial injury often results in an accumulation of macroscopic thrombi in the veins.

In a sense, thrombus formation at the site of injury is like normal cicatrization of a dermal wound. In a patient with increased coagulation or defective anticoagulation, thrombus formation can be overly exuberant, similar to the formation of a hypertrophic scar. If fibrinolysis is inhibited, the thrombus extends away from the area of the original vascular injury to invade areas of normal endothelium, similarly to keloid formation. Disorders of hemostasis, coagulation, anticoagulation, or fibrinolysis occur in a variety of clinical settings that can cause recurrent DVT or PE and premature arteriosclerotic syndromes or myocardial infarction at an early age.

Hemostasis

The initiating event in venous thrombosis is platelet adhesion. Even minimal vascular endothelial injury reliably initiates a predictable sequence of events that results in platelet adhesion and thrombus formation. Initial platelet adhesion and aggregation are stimulated by a component of endothelial cells, most likely a substance known as amorphous electron-dense substance, which is exposed by endothelial cell injury. The release of this substance is enhanced by activity of the intrinsic coagulation cascade and is inhibited by platelet antiaggregating agents, thrombolytics, and anticoagulants.

Platelet activation causes the release of platelet proaggregants thromboxane A2 and serotonin, resulting in the aggressive recruitment of more circulating platelets to form a hemostatic plug. Thromboxane A2 and serotonin also act to bring about local vasoconstriction. Exposed platelet membrane phospholipids catalyze the activation of factor X and the local (endothelial) formation of thrombin, itself a powerful proaggregant. Thrombin-mediated platelet aggregation is unaffected by aspirin and nonsteroidal anti-inflammatory agents, but aggregation caused by platelet-derived thromboxane A2 is dependent on platelet cyclooxygenase, which is reversibly inhibited by nonsteroidal anti-inflammatory agents and is irreversibly inhibited by aspirin.

Coagulation

After a hemostatic plug is well established, coagulation pathways are activated and thrombin is generated. Fibrin cross-linking builds a true thrombus out of what was initially a loose aggregation of blood elements. If this series of events were unopposed, any small vascular endothelial injury would result in thrombus propagation throughout the venous system. Three factors serve to retard and prevent uncontrolled propagation: flow dilution, natural anticoagulants, and natural thrombolytics. If blood flow is reduced, activated coagulation factors will accumulate rather than be carried away. If this happens or if some defect is present in the production or function of the natural anticoagulants or thrombolytics, the thrombus forms more vigorously than appropriate for a given vascular injury. The patient develops recurrent venous thrombosis and PTE.

Anticoagulation

Protein C, protein S, and antithrombin III are the best understood of the natural circulating anticoagulants. Antithrombin III, which interferes with the action of serine proteases such as thrombin, is a general inhibitor of the intrinsic pathway. Protein C (with its cofactor, protein S) inhibits factor V and factor VIII, principal components of the common coagulation pathway.

Paradoxically, a functional deficiency of the procoagulant factor V increases resistance to the anticoagulant effects of activated protein C. This deficiency is present in nearly half the patients with clinically recognized venous thrombosis. Many other plasma proteins serve as activators, inhibitors, or cofactors in the coagulation cascade, including such known proteases as heparin cofactor II, alpha2-macroglobulin, alpha1-antitrypsin, and C1 inhibitor. Isolated deficiency of heparin cofactor II can cause recurrent venous thrombosis, and other cofactors can increase the likelihood of thrombosis in response to vascular injury or venous stasis. Together, these plasma proteins prevent minor endothelial injury from initiating uncontrolled intravascular coagulation.

Fibrinolysis

Fibrinolysis is the body's defense against the formation of a thrombus. Fibrinolysis is initiated by tissue activators and by circulating activators that transform the inactive precursor plasminogen into the active fibrinolytic agent plasmin. Plasmin attacks and degrades fibrin, and when excess plasmin is present, it also attacks and degrades fibrinogen. Damaged endothelial cells release tissue-type plasminogen activator at the same time they bind platelets and initiate the clotting process. This balancing process ensures that under normal conditions, the formation of a thrombus remains localized to an injured area where it is needed. Any disturbance of the delicate balance leads either to increased bleeding or to increased propagation of thrombi.

The principal physiologic plasminogen activators are urokinase-type plasminogen activator and tissue-type plasminogen activator. The latter is found in the endothelial cells of vein walls and is released in response to physiologic stimuli such as segmental venous stasis, vessel wall injury, exercise, and the presence of thrombin. Most of the action of tissue-type plasminogen activator occurs at the surface of a thrombus, where plasmin is formed after plasminogen and tissue-type plasminogen activator together bind to fibrin. However, circulating tissue-type plasminogen activator produces a systemic lytic state in which circulating fibrinogen is consumed.

Impaired fibrinolytic activity permits thrombus propagation and leads to an increased likelihood of clinically apparent venous thrombosis. Many different problems can interfere with fibrinolysis. Plasminogen levels may be low, or plasminogen may be defective because of structural abnormalities. Fibrinogen and fibrin may be structurally abnormal in such a way as to resist degradation by plasmin. A patient may have high levels of circulating inhibitors of fibrinolysis or low levels of plasminogen activators.

Clinical: The clinical diagnosis of DVT is difficult and fraught with uncertainty. The classic signs and symptoms of DVT are those associated with obstruction to venous drainage and include pain, tenderness, and unilateral leg swelling. Other associated nonspecific findings are warmth, erythema, a palpable cord, pain upon passive dorsiflexion of the foot, and spontaneous maintenance of the relaxed foot in abnormal plantar flexion (the Homan sign). When a patient presents with these symptoms, the diagnosis of venous thrombosis is strongly suggested, but no patient should be treated based on clinical findings alone because even when a patient has a swollen, painful, congested leg that appears to be clinically obvious DVT, the chance that DVT is the correct diagnosis is only 50%.

Conversely, an absence of signs and symptoms does not rule out DVT. Most cases of DVT lack classic signs or symptoms, and thus, DVT is not considered. Only 7% of postoperative renal transplantation patients, for example, display clinical symptoms of DVT, yet prospective investigation leads to the diagnosis in 20% of cases. DVT simply cannot be diagnosed or excluded based on clinical findings; thus, diagnostic tests must be performed whenever the diagnosis of DVT is being considered.

When a patient has DVT, symptoms may be present or absent, unilateral or bilateral, or mild or severe. Thrombus that does not cause a net venous outflow obstruction is often asymptomatic. Thrombus that involves the iliac bifurcation, the pelvic veins, or the vena cava produces leg edema that usually is bilateral rather than unilateral. High partial obstruction often produces mild bilateral edema that is mistaken for the dependent edema of right-sided heart failure, fluid overload, or hepatic or renal insufficiency.

Severe venous congestion produces a clinical appearance that can be indistinguishable from the appearance of cellulitis. Patients with a warm, swollen, tender leg should be evaluated for both cellulitis and DVT because patients with primary DVT often develop a secondary cellulitis, while patients with primary cellulitis often develop a secondary DVT. Superficial thrombophlebitis, likewise, is often associated with clinically inapparent underlying DVT.

If a patient is thought to have PE or has documented PE, the absence of tenderness, erythema, edema, or a palpable cord upon examination of the lower extremities does not rule out thrombophlebitis, nor does it imply a source other than a leg vein. More than two thirds of patients with proven PTE lack any clinically evident phlebitis. Nearly one third of patients with proven PE have no identifiable source of DVT despite a thorough investigation. Autopsy studies suggest that even when the source is clinically inapparent, it lies undetected within the deep venous system of the lower extremity and pelvis in 90% of cases.

DVT below the knee

Although DVT below the knee is widely believed to be benign, this is untrue. Most cases of proximal DVT have their origins in the venous sinuses of the calf, and propagation to the popliteal vein and the femoral vein occurs in 20-30% of cases. However, DVT need not spread proximally to cause fatal PE. The single largest autopsy series ever performed to specifically to look for the source of fatal PE was performed by Havig in 1977, who found that one third of the fatal emboli arose directly from the calf veins.

The lower leg has 3 principal pairs of deep veins: the anterior tibial vein, draining the dorsum of the foot; the posterior tibial vein, draining the sole of the foot; and the peroneal vein, draining the lateral aspect of the foot. DVT that is isolated to the anterior tibial vein results in PTE in 30% of cases and is responsible for many deaths. Other deep vein groups draining the lower leg include the gastrocnemius plexus and the soleal plexus. These plexuses and the deep venous groups named above all drain via the popliteal vein at the knee. Thrombosis of the popliteal vein results in PTE in 66% of cases, a frequency similar to that of DVT in the thigh.

Calf deep vein thrombophlebitis is an important cause of morbidity quite aside from any risk of propagation or of embolization. Isolated calf vein thrombophlebitis results in clinical postphlebitic syndrome in 20-40% of cases. The pathophysiology of the postphlebitic syndrome has been well established as one in which the recanalization of thrombosed deep veins results in the destruction of the venous valves, leading to chronically elevated ambulatory venous pressure within the legs. Valve incompetence need not be extensive to produce venous hypertension and clinical symptoms. Isolated incompetence of the valves in the popliteal segments of the deep venous system leads to elevated ambulatory venous pressures averaging 72 mm Hg, and more than 60% of those with isolated popliteal valve failure develop severe clinical signs of chronic venous insufficiency (CVI). This postphlebitic syndrome is responsible for chronic pain, edema, hyperpigmentation, and ulceration and for many cases of recurrent DVT and PE.

Questions and Answers with Doctors About DVT

These comments are made for the purpose of discussion and should NOT be used as recommendations for or against therapies or other treatments. An individual patient is always advised to consult their own physician.

Hemotoma [posted 1/13/99] 
Question: What is the treatment I should be having for a hemotoma? My doctor just looked at it and said it was a "design fault" - i.e. because humans are bipedal the blood collects there. She did not recommend any treatment, but I am a bit concerned about it to say the least.

Answer: Treatment for a hemotoma is usually heat to absorb the blood in the damaged tissue. As to a design fault, hemotoma is a medical name for a bruise. I'm not sure I'm answering your question.

Blood Clots and Birth Control [posted 1/8/99] 
Question: I was hoping to find someone who could answer a question for me on blood clots and the pill. Do you know where I could look?

Answer: I can give you some information, but the companies that produce them have tons.

Possibly Post Phlebitic Syndrome [posted 1/6/99] 
Question: If I still have a blood clot in my calf, and my doctor takes me off of coumadin, what are my chances the blood clot will go o my lungs? If it is Post Phlebitic Syndrome, what can I do to relieve the pain I have in my calf and foot? Is there a medication I could try to alleviate this? Also is this going to be with me for the rest of my life? Will it ever get any better.

Answer: Clots below the calf may embolize, but rarely, if ever, cause symptoms. This is probably due to the size of the clot and the low risk of embolization. However, they can and do cause chronic pain after the clot referred to as Post Phlebitic Syndrome. This is distension and inflammation of the veins in the leg is due to damage to the venous valve structure of the leg. This tends to be permanent since the cause is incompetent valves, which leak blood back to the leg causing chronic distension and pain. Relief centers on compression stocking, aspirin on a daily basis, elevation of the painful calf (above the heart) and heat.

Blood Clots [posted 10/13/98] 
Question: My husband,26, has had three clots in his lower leg in the past two years. They are all injury related. He takes an aspirin a day but clots each time he receives a hard hit to the leg. The doctors have tested him for any factors that may cause this. They turned up nothing. Could these clots over time cause more serious problems for his legs?

Answer: Yes, especially if in the deep venous system-has he been tested for Factor V Leiden activity? A newer and very common cause of clotting disorders.

Blood Clots [posted 8/11/98] 
Question: My brother recently had a pulmonary embolism due to a blood clot discovered in his leg. His trouble breathing started after scuba diving in December. Could this have cased the blood clot?

Answer: Possible, but unlikely. If he is young, he should have a work-up by a good internist or hematologist for the familial causes of hypercoagulability. This is important because it can prevent further problems in the rest of the family if found.

Blood Clots 
Question: My husband was in a motorcycle accident 5 yrs. ago. He has post concussion syndrome and is currently seeing a psychologist as he has difficulty relaxing. Last year he had bluetoe or a blood clot in his little toe. At this time he had his collarbone rebroke and a steelplate added. He also, during the same time, had die injected and a scope put in his vein. Just recently he had bluetoe again. They did another scope and also put in a shunt. This helped the blood pressure in his hip; however, he now has bluetoe again. He is having a difficult time quitting smoking, even if they may have to amputate. His mother had phlebitis, and heart problems run in his family. Is there anything he can do to correct the blood coagulation?

Answer: The physical problems caused by the accident are probably contributing to his problem but are probably not the cause. He needs to stop smoking. Occasionally, use of a drug like procardia will help peripheral vasodilation sufficiently to stop the problem.

Blood Clots 
Question: I need to know information with regards to blood clots in the legs associated with chemotherapy and also the need to amputate any part of the leg after clots have been operated on.

Answer: There are two possible types of clots in the legs - arterial and venous. Arterial clots are usually due to emboli from the heart. However, some patients experience hypercoagulability with different types of cancers and can form arterial clots in different parts of the body. Few chemotherapy agents would cause this problem, and usually the reverse. Venous clots usually form in the leg and can go to the lung in severe cases. These are due to low flow in the legs or else the hypercoagable state I mentioned with different cancers. Venous clots do not usually require amputation. Arterial occasionally due if not correctable rapidly.

Blood clots 
Question: I'm a 28 year old that got a blood clot about 2 years ago, supposedly from lifting weights. The clot is in my main vein of my left arm. Collateral veins have since grown around the clotted off spot and provide for full functions on the arm. When the clot occurred I had it successfully dissolved, (heprin, veniogram and angioplasty) but several days after I returned home from the hospital the clot returned. This time my doctor wanted to try a rib resection to relieve the pressure on the vein. This was done about 2 weeks after the clot had returned and was followed by another attempt to remove the clot using veniograms and eurokinates (sic). However, this was not successful. The doctor says that once a clot becomes hard it is almost impossible to remove and even if it were removed the vein may become injured and another clot occur. I was released from the hospital and am not on any kind of medication, nor make regular visits to my doctor. Supposedly, a hardened blood clot is not much to worry about and it will slowly dissolve itself over time. If it did break loose, I was told I would probably survive it. A major problem for me is that my unclotted right arm is missing 5 fingers due to a birth defect, so I am somewhat reliant on the clotted arm. Does what I just said fit into the standard medical blood clot treatment that you may advocate?
Do you recommend continuing my active lifestyle? (exercise, an occasional triathlon, occasionally fight wildland forest fires, lift weights, etc...)
What are the signs that my clot is breaking loose (embolism?) and what are the chances of this happening?
What could I do to help myself as I await medical help? (lie quietly, rush to hospital, take medications, etc....)

Answer: When blood clots occur in young people the question is why? Birth control pills, steroids trauma, inactivity and some inherited disorders could be the initiator of a clot. So, first ensure your physician has screened you for Protein C, Protein S, Lupus coagulants Antithrombin III and checked your platelet count, etc. If the above are normal, I'd recommend an aspirin a day to avoid any further clots. The damage to your arm is of no consequence. The arm has several pathways to return blood other than that one vein. Emboli from the arm are rare and never cause majorage. Continue exercising. Signs of a blood clot in the lung are either chest pain (usually pleuritic), hemoptsis (spitting up blood), or shortness of breath, but unless you develop a clot in the leg you are at minimal or no risk.

Blood clots 
Question: Is there any treatment for severe venous occlusion of the legs (inferior vena cava, both iliacs and messentaric)? A greenfield filter is in place. I am on Coumadin but I have severe pain in both my legs.

Answer: Your problem is called post-phlebitic syndrome. It occurs after damage and scarring to the venous structure of your legs caused by the clots. The best treatment is to dissolve the clot as soon as possible after it occurs with any of several drugs. Unfortunately, once the clot has been present more than a couple of days or the damage present, there is no effective treatment. Treatment centers on pressure stockings for your legs and elevation of the legs several times a day. Occasionally, anti-inflammatories (after decreasing the coumadin, ifpossible) are helpful. This is a tough problem to improve because the treatment options are very limited.

Poor blood flow 
Question: I have recently developed muscle cramps in my calf muscles, which tighten over short periods of walking and are pronounced when I add weight (carrying an object of some 40-50 pounds). Is there a medication that will ease or substantially eliminate the symptom?

I am also curious about what may be available to permit a senior citizen of advanced years to resume sexual activity that is denied because of a lack of ability to sustain an erection of sufficient firmness. I am 72 years old and an inveterate smoker (2-4 packs a day).

Answer: This is called claudication. There are several possibilities, but generally in smokers it is due to lack of blood flow to the legs. With your decreased erections I suspect you have a major league blockage of the iliac and/or femoral arteries. Your physician will need to get arterial studies to check this. The other possibility is spinal stenosis. This is caused by pressure on the spinal cord in the lower back due to a congenitally small opening in the spinal canal. Regarding your erections, have your blood supply to your legs checked first. The lack of erections are probably due to a similar problem.

Clots In Legs 
Question: Why would a man in his late thirties experience two different blood clots in his leg?

Answer: There are several reasons that a person forms clots in his/her legs. The most common reason is trauma or inactivity. Clots following a fractured leg or immobilization of the leg for any reason are relatively common. In a thirty year old there are also several syndromes which are inherited in families. A complete evaluation by a physician will be necessary to check the blood for the known causes of inherited tendencies to clot. Also, once a person has one clot-the damage caused to the venous system will markedly increase the tendency for a second clot. 

Vascular Suregon and Family Doctor Say No To Diving with DVT's

Vascular Suregon and Family Doctor Say No To Diving with DVT's
After investing $500 in classes and $700 in equipment I find out that I can not go scuba diving with my DVT condition.

Contrary to everything I read online, in reality if you have a good Doctor they are going to say. My doctor explained in detail why and I will try to do my best to reguritate that information for readers thinking of diving with blood clots.

First of all if you have blood clots in your leg, then you more than likely have them in your lungs also. This is known as a pulminary embolism. This alone makes it dangerous to dive and it is listed on the medical approval form for NAUI as a condition that will make it risky for you to dive.

Second of all, if you have blood clots in your lungs and legs then you more than likely have a few in your brain and that makes its really risky to dive with DVT or blood clots.

My Vascular surgeon said he has approved people to go 15 and 20 feet but highly recommended that I opstain from diving becuase of the many risks.

Finally, with the Venal Cava Umbrella I have is not rated for diving. I am doing research on this now and will post more but the vascular surgeon says it says it on the box to not exceed 10-15 feet underwater on it. (more info on Venal Cava Umbrella)

The Squeeze - High Cholesterol and Deep Vein Thrombosis (DVT)

The Squeeze - High Cholesterol and Deep Vein Thrombosis (DVT)

I just came back from my doctor who told me of an interesting problem that I am having. I have not researched it as of yet but I am sure there is not a lot of information about having high Cholesterol and DVT (Deep Vein Thrombosis)

THe question came up when I asked her about my desire to get off coumadin (warafin). She told me that with my high cholesterol and with my think blood that likes to clot that it would be a dangerous transistion.

Basically I have a vascular squeeze going on. If my arties are think with cholesterol and my blood is thick, then we have a squeeze.

I will be researching this and trying to bring my cholesterol levels down with diet and exercise. My doctor gave me 6 weeks to do it.

At my last physical my Cholesterol levels were as follows:

My Triglycerides are 260. The range that I should be in is 0 to 150!

My LDL Cholesterol is 176.

My HDL Cholesterol is 31. The range that I should be in is 40 to 135. Can bring this up with exercise.

My Cholesterterol score is 259 and the range I should be in is 140-199.

What I Believe Caused My DVT

I have been told its a vitamin K deficiency is the cause of my blood clots but I believe it was caused from falling through my newly renovated floor. I have went to two specialist and one primary doctor who have all told me different things. I should do more research on my own. I do not want to take rat poison (warafin) for the rest of my life.

I found this article and though it was relevant:

Minor Leg Injuries Might Boost Blood Clot Risk
Thu Jan 17, 5:02 PM ET
THURSDAY, Jan. 17 (HealthDay News) -- Minor leg injures -- including ankle sprains and muscle ruptures -- could raise the risk of blood clots in the legs or lungs, suggests a study by researchers in the Netherlands.

Previous research found that major injuries and related treatments such as surgery, a plaster cast, and extended bed rest increase the risk of venous thrombosis, which includes blood clots in the leg as well as more dangerous blood clots that have traveled to the lungs (pulmonary embolism). But the risk associated with minor leg injuries was unknown.

In this study, the researchers at Leiden University Medical Center studied almost 2,500 people who developed venous thrombosis between 1999 and 2004. They compared those patients with a control group of more than 3,500 people without venous thrombosis.

They found that 289 (11.7 percent) of the patients had sustained a minor injury in the three months prior to developing venous thrombosis, while just 154 (4.4 percent) of those in the control group had a minor injury in the three months before the study.

"Minor injuries that do not require surgery, a plaster cast or extended bed rest were associated with a threefold greater relative risk of venous thrombosis," the study authors wrote.

"The association appeared local, because injuries in the leg were associated strongly with thrombosis, while injuries in other locations were not associated with thrombosis. The association was strongest for injuries that occurred in the month before the venous thrombosis, suggesting a transient effect."

The researchers also found the association was stronger in people with genetic or other risk factors for blood clots.

The study was published in the Jan. 14 issue of the journal Archives of Internal Medicine.

More information

The Society of Interventional Radiology has more about deep vein thrombosis.

Swelling After Surgery

Well it was interesting after getting out of the hospital how much swelling I encountered in my leg. The doctor told me to expect this but I have to say it was a little shocking. It looked more like pooling of blood in my leg than swelling. My leg was very dry (or ashy) and the overall shape of my lower leg became distorted.

The good news is that as time went on this swelling got less noticeable (a couple of years later). Even though it became less noticeable every now and then I it seems to swell more than at other times. The doctor told me that this could be my body passing clots throughout my system. I think it is more timed around me forget to take my coumadin.

I want to get off this stuff because taking a pill every day at 36 is no fun.

What I thought Was A leg cramp was a blood clot (or Deep Vein Thrombosis)

I remember how it felt, a tightness in my upper thigh. I thought I had pulled my groin muscle or something. The worst thing that I did was wait. No one tells you what these things feel like. And when they do they use complex descriptions.

I will tell you that the blood clot I had felt like I had a pulled muscle.

I was walking around it for days. I even had my friend massage this "pulled muscle." When I think about it, it kind of makes me cringe. My friend sitting there rubbing this deadly blood clot in my leg, yuck. If it was massage the right way I a sure and the doctors where sure that it would have killed me.

This tightness was the blood being restricted in my veins by the clot.

If you feel this tightness in your extremities (arms or legs) go to a hospital immediately.

I made the mistake of going to an urgent care facility. They misdiagnosed it completely ...