AWSOME WEBBLOG ABOUT AN ACTIVE YOUNG GUY WITH DVT

http://www.hentzel.com/clot.htm

http://www.hentzel.com/dvt_diary.htm

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.

Very Relevant Article I found with a person who has a similar DVT Situation

'Sticky' blood cause for concern

The Monterey County Herald
Article Last Updated: 04/12/2008 01:59:24 AM PDT

Dear Dr. Gott: I am a 61-year-old male with no heart problems or recent surgeries. In June 2004, I developed a blood clot in my left lower leg, which then resulted in a pulmonary embolus (clot) in my right lung.
I was admitted to my local VA hospital and put on 5 milligrams Coumadin daily. My PT/INR was kept in the 2.0 to 3.0 range. I continued the medication until October 2006, when I was told I could stop it.

All was well until February 2007, when I developed multiple pulmonary emboli in both lungs. This time, I did not have any of the leg symptoms.

I again went to the VA hospital, where I was put on 5 milligrams of Coumadin every day. I was told that I would have to take it for the rest of my life.

Because I did not understand why this was happening, I made an appointment with a hematologist (blood specialist). She took blood samples and did a genetic profile. Everything came back negative or normal. She concluded that I now have naturally "clotty" blood and I would have to live with it. There was no identifiable cause.

Why, after 58 years of being a "normal blood clotter," did the above happen to me? Will I really have to be on Coumadin for the rest of my life? Should the VA doctors be doing more for me? Your opinions are appreciated.
Dear Reader: I don't know why your blood is now clotting dangerously. Your hematologist appears to have run extensive tests and ruled out genetic factors and disorders as the cause.

You will need to continue the Coumadin for the rest of your life. If you discontinue it, you will run a very high risk of developing more pulmonary emboli (blood clots in the lungs). You would also be at higher risk for heart attack and stroke if the clots broke off and were carried to your heart or brain. "Sticky" blood is especially dangerous, and your physicians have taken appropriate steps to normalize your blood and reduce the risk of serious consequences.
Another option, albeit unlikely, to explore is lung cancer. In my practice, I have seen several cases in which pulmonary emboli were the only symptoms of lung cancer.

If you want to explore this option, I recommend you see a pulmonologist (lung specialist). He will most likely take a medical history, do an examination and order some imaging studies of your lungs.

Let me know what happens.

To give you related information, I am sending you a copy of my Health Report "Pulmonary Disease." Other readers who would like a copy should send a self-addressed, stamped number 10 envelope and $2 to Newsletter, Box 167, Wickliffe, OH 44092. Be sure to mention the title.

Write to Dr. Gott c/o United Media, 200 Madison Ave., 4th fl., New York, N.Y. 10016.

COLUMN SIG IN STORAGE DESK under GOTT

Anxiety Linked To Blood Clots: Fear That Freezes The Blood In Your Veins

ScienceDaily (Mar. 26, 2008) — "The blood froze in my veins" or "My blood curdled" -- these common figures of speech can be taken literally, according to the latest studies. Indeed, more literally than some of us would like. For it turns out that intense fear and panic attacks can really make our blood clot and increase the risk of thrombosis or heart attack.
Earlier studies showed that stress and anxiety can influence coagulation. However, they were based almost entirely on questionnaire surveys of healthy subjects. In contrast, the Bonn-based research team around Franziska Geiser (from the Clinic and Policlinic for Psychosomatic Medicine and Psychotherapy) and Ursula Harbrecht (from the Institute of Experimental Haematology and Transfusion Medicine) have been the first to conduct a very careful examination of coagulation in patients with anxiety disorders.
Everyone experiences anxiety from time to time -- fear of failing the math's test, dread of going down into the dark cellar or, in a more general sense, trepidation about what the future holds. But some people are gripped by powerful fears when confronted by quite normal everyday situations. For example, sufferers of agoraphobia frequently have panic attacks when caught up in a crowd.
The symptoms can be dramatic: palpitations, sweating, shaking, blind panic or fainting -- even leading to death. Another anxiety disorder frequently encountered can be described as social phobia. Those affected fear above all situations in which they become the centre of attention in a group. They begin to stutter or turn red. In order not to avoid embarrassment, social phobia sufferers may become recluses, shying away from human contact and staying at home.
The medical researchers in Bonn compared patients who suffer from a severe form of panic disorder or a social phobia with a healthy control group. In order to rule out as far as possible the influence of factors like age and sex, each of the 31 patients with anxiety disorders was matched with a corresponding healthy patient of the same age and sex. The subjects first had to give blood samples and were asked to perform a number of tests on the computer. A second blood sample was then taken. The blood analysis, which measured various coagulation factors, produced a clear result: The group of anxiety patients showed a much more highly activated coagulation system than the healthy control group.
In the coagulation system two mechanisms operate that are indispensable to life and normally work in opposite directions, each counterbalancing the other. On the one hand, coagulation involves a thickening of the blood so that a plug can form and prevent excessive bleeding from damaged vessels. On the other hand, there is "fibrinolysis", a process that keeps the blood fluid and breaks down clots. In the case of the anxiety-disorder patients, however, the researchers observed through close analysis of the blood an activation of coagulation accompanied by an inhibition of fibrinolysis. Yet, apart from the prick for blood sampling, no real injury had occurred. For these types of patients, the coagulation system goes out of balance as the coagulation tendency rises -- possibly with dangerous consequences. In extreme cases the imbalance can lead to blockage of a coronary artery.
The increased coagulation tendency could, says Franziska Geiser, be the "missing link" that explains why anxiety patients have a statistically higher risk of dying from heart disease by a factor of 3 or 4. "Of course, this doesn't mean that every patient with a marked anxiety disorder must now worry about having a heart attack. The coagulation values we measured were always within the physiological scale, which means there is no acute danger," adds the project leader. A real health threat only arises when other risk factors, like smoking and obesity, also come into the equation.
Franziska Geiser also has some good news for people with anxiety disorders. A follow-up study has produced the first evidence that coagulation activation subsides in patients who have completed successful therapy for their condition. In this respect, Dr. Geiser calls for earlier diagnosis of anxiety disorders, pointing out that too much time is wasted before effective psychotherapy is prescribed. "After all, we have programmes to help the population give up smoking or take more exercise. But if we want to reduce the number of heart disorders, it would make sense to improve the way anxiety disorders are diagnosed and treated."
Adapted from materials provided by University of Bonn.

Awsome Diving Info. and Why Its Bad for People With IVC's or DVT's

http://archive.rubicon-foundation.org/dspace/bitstream/123456789/3933/1/ASCP4057_Handout.pdf

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.

Interesting Article on Scuba Diving With Medical Equipment like Vena Cava Filter

Medical Implants
Questions are posed concerning the integrity of medical appliances when exposed to the increased barometric pressures associated with SCUBA diving. Many individuals with disabilities such as spina bifida have connections between the brain anf the abdominal cavity (ventriculoperitoneal shunts) for the treatment of hydrocephalus (excessive fluid on the brain). Huang et al.10 subjected four ventriculoperitoneal shunts to one and four atmosphere absolute in a hyperbaric chamber and found that all shunts performed according to manufacturers’ specifications. They reasoned that any increase in pressure will compress all fluid-filled compartments. Therefore, there would be no significant change in gradient between intracranial and intraperitoneal pressures. Preliminary studies have been carried out for cochlear implants in a hyperbaric chamber, illustrating that the implantable components of various cochlear implants can withstand pressures of up to six atmospheres without damage or failure of critical seals.11

Intrathecal baclofen pumps are increasingly being utilized in the management of spasticity and dystonia. Akman et al.12 described a case of retrograde leakage of cerebrospinal fluid (CSF) into the infusion pump reservoir of an intrathecal baclofen pump (Medtronic SynchroMed, Medtronic, Minneapolis, MN) during hyperbaric oxygen therapy. Medtronic does not recommend exposing their intrathecal baclofen pumps to pressures of 2 atmospheres absolute (SynchroMed II Technical Manual, Medtronic).

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. 

What is a Vena Cava Filter and How Does this filter help with DVT's and blood clots

Okay I finally am getting to the topic of machinery that they installed in my body. First off let me give a little history. I had a blood clot in my leg that felt like a severe muscle cramp or pulled muscle. I went into to get it removed and was put on Heprin. 

I was release from the hospital and formed another blood clot. I was readmitted to the hospital and was put on heprin again. This time the doctors decided to install a Vena Cava filter in me.

I was surprised to find out this device does limit diving even though I can find no eveidence of this anywhere  (the doctor says the warning is on the box) . I will be calling their offices to make sure this is the case.

This is what the filter looks like:

Well anyways this Braun filter that they installed in me has the potential to stop a floating blood clot from going into my lungs and brain. Even though the doctor told me that I have blood clots already in my lungs and more than likely have some in my brain, I guess this is just a precautionary procedure to stop more from coming in.

This is how it works (click the image  below to make it bigger):

Check out these links for in-depth information and clinical trials with this filter. These links were not easy to find:

In Vitro Evaluation of a New Vena Cava Filter

Braun the company that makes the device I have in me - Vena Cava Filter LP

Lipitor: Side Effects And Natural Remedy

Serious side effects have been reported for Lipitor and other cholesterol-lowering drugs - the so-called statins - prescribed to millions for preventive purposes. The prescription of these drugs is based on the discredited hypothesis that high cholesterol levels cause heart attacks. The cholesterol myth has been one of the most long lived falsehoods around - probably because it has been excellent business, both for large pharma producers as well as for the food multinationals, who introduced margarine telling us how much healthier it is than butter.

There is an easy, widely available nutritional solution to heart attacks: Vitamin C. Needless to say, taking more vitamin C has been opposed by big pharma and its mainstream medicine followers for decades.

When a "preventive" medicine causes severe muscular degeneration as a "common" side effect, something must be awfully wrong. Jonathan Campbell examines the side effects and postulates a mechanism - proposing an astonishingly simple remedy.

Lipitor - Reports of Neuromuscular Degeneration
by Jonathan Campbell, March 16, 2004

Numerous adverse side effect reports have implicated Lipitor as a possible cause for severe neuromuscular degeneration. Some people who have been using Lipitor for two years or more report symptoms similar to multiple sclerosis or ALS - Lou Gehrig's Disease - in which they are losing neuromuscular control of their bodies.

For instance, in an article entitled "Life After Lipitor" that appeared in the newspaper Tahoe World on January 27, 2004, Tahoe City (California) resident Doug Peterson began having serious neuromuscular problems after taking Lipitor for two years. He began losing muscular coordination and slurring words when he spoke. Then he lost balance, followed by loss of fine motor skills - he had difficulty writing. He went from doctor to doctor, trying to figure out what could be happening. Finally one doctor suggested that he stop taking Lipitor, and the downward health spiral stopped and his health is now slowly improving.

READ MORE HERE

Don't Take Crestor For Cholesterol

As the readers know I have DVT, A High Likelihood of Pulmonary Embolisms, and High Cholesterol

My dad mentioned that taking statins can hurt your kidneys this is what I found so far:

NEWSLETTER 11: BAD CRESTOR

Crestor Rhabdomyolysis

Rhabdomyolysis is a life-threatening muscle deterioration that is associated with statin type of cholesterol lowering medication like Crestor. AstraZeneca's NDA (new drug application) with the FDA for Crestor was initially delayed when the company halted clinical trials worldwide after reports of kidney damage, death and muscle weakness (an early signal for rhabdomyolysis) in clinical trials in patients taking 80 milligrams of Crestor per day. Crestor labeling includes warnings about the potential for muscle and kidney problems, including rhabdomyolysis, but warning labels arguably may not be adequate and sufficient enough to convey the seriousness of the severe side effects that can occur from Crestor use. Crestor is the only statin that is known to have caused rhabdomyolysis in pre-approval clinical trials. Rare cases of rhabdomyolysis with acute renal failure secondary to myoglobinuria [a protein from muscle] have been reported with rosuvastatin and with other drugs in this class. The professional product labeling goes on to instruct physicians to tell patients "... to promptly report unexplained muscle pain, tenderness, or weakness, particularly if accompanied by malaise or fever." The risk of muscle damage leading to rhabdomyolysis during treatment with rosuvastatin may be increased when it is used together with other cholesterol-lowering drugs and cyclosporine (NEORAL, SANDIMMUNE), a drug used after transplantation to prevent organ rejection. A single rosuvastatin dose given to healthy volunteers along with the cholesterol-lowering drug gemfibrozil (LOPID) resulted in a significant increase in the amount of rosuvastatin in the body. There is a bolded statement in the Warnings section of rosuvastatin's labeling stating that "Combination therapy with rosuvastatin and gemfibrozil should generally be avoided." The risk of muscle problems possibly leading to rhabdomyolysis is also increased when niacin is used to lower cholesterol in combination with rosuvastatin. Crestor, a member of a class of cholesterol-lowering drugs commonly referred to as "statins", was approved in the U.S. in August 2003, and based on review of an extensive clinical database involving approximately 12,000 patients. "Myopathy/Rhabdomyolysis" increased risk in: increased age, hypothyroidism; renal insufficiency. Physicians are warned to prescribe Crestor with caution in these patients, particularly at higher doses, as the risk of myopathy increases with higher drug levels. In addition, the U.S. approved labeling for Crestor states that increased rosuvastatin drug levels were observed in certain sub-populations of patients (ie: subgroups of Asians, patients concomitantly using cyclosporine and gemfibrozil), conferring increased risk of myopathy. Because of these findings, the FDA required Astra-Zeneca to make available in the U.S. a 5-mg dose that could be used in patients requiring less aggressive cholesterol-lowering, or who were taking concurrent cyclosporine. The maximum recommended dose in the FDA-approved label is limited to 10-mg daily in patients with severe renal impairment or who are also taking gemfibrozil. To date, seven patients using Crestor (rosuvastatin) are known to have developed a deteriorative muscle condition known as rhabdomyolysis, and nine others have suffered kidney damage or failure. Even the death of a 39 year old woman isn't enough for the FDA to ban Crestor.

Some people claim that Crestor has dangerous side effects such as proteinuria (protein in the urine) and rhabdomyolysis, (a dangerous condition where the muscles break down and release toxic chemicals into the bloodstream that hurt the kidneys). For Crestor, there were about 13 reports of rhabdomyolysis for every million prescriptions filled, Public Citizen estimated. That rate was 6.2 times higher than the rates for all other statins combined.

READ MORE HERE

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)

Diet to Lower Your Cholesterol

Low Cholesterol Diet
Fat is a major energy source for the body. However, it is not the body's only source of energy, and too much fat in the diet can be harmful. It is especially bad for the circulatory system because it raises blood cholesterol levels that can contribute to heart attack or stroke.

These diets are designed to reduce fat and cholesterol to levels recommended by the National Cholesterol Education Program (NCEP). NCEP is made up of 40 private and governmental groups coordinated by the National Heart, Lung, and Blood Institute. Both diets have the following goals:

• decrease total dietary fat, especially saturated fat
• decrease dietary cholesterol
• limit sodium intake
• increase intake of fiber and complex carbohydrates
• decrease calories if needed to reach a healthy body weight

read more here http://www.gicare.com/pated/edtot24.htm

Wow first link found on DVT and high cholesterol very disturbing...

Wow first link found on DVT and high cholesterol very disturbing...

http://www.dvt.net/allAboutDVT/cardioHealthDVT/default.aspx

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.

Articles on Diving With DVT

Unbiased Collection Of Posts and Articles on Scuba Diving With DVT. I hope it helps you draw your own opinion. Please make sure you check with your physician because as my Naui instructor told me any drugs you are on (like blood thinners) while scuba diving might not work as effectively while scuba diving.

1) MedToGo - owned and operated by US physicians Says No To Diving If You Have Had Previous Blood Clots : " ... but blood clots or previous blood clots in the deep veins of the legs (deep venous thrombosis) or the lungs (pulmonary embolism) will eliminate you from diving."

2) Scuba Board exchange on diving with DVT

3) Scuba Diving with DVT and anti coagulants

4) Scuba Diving After A Blood Clot

5) Scuba Board discussion on Coumodin and Diving

6) Good Exchange of Diving with DVT

7) Information on Diving and Warafin

8) Warafin and Diving - Doctor Says Not For It

9) London Article on Diving with DVT

10) Good post on Diving with DVt and possible cascading affects

Wear Compression Stocking When Traveling With DVT and To Prevent DVT

Garments called "graduated compression stockings" greatly decrease the risk of dangerous blood clots called deep vein thrombosis (DVT) for passengers on long-haul flights, a new study finds.

In fact, researchers found that individuals who do not wear these stockings when they fly are 12.5 times more likely to develop a potentially fatal DVT than people who do wear them. The review, published in the current issue of the Journal of Advanced Nursing, focused on the results of nine comparative trials involving about 2,500 airline passengers. Only two of the 1,237 people who wore compression stockings developed DVT, compared with 46 of the 1,245 people who didn't wear the stockings, according to researchers at Fooyin University, Taiwan.

All the study participants were advised to walk or exercise regularly during their flights, drink water, avoid salty food, and to make sure that carry-on luggage didn't restrict their leg movement.

Although the compression stockings reduced the risk of DVT, they had little effect on the incidence of a less-serious condition called superficial venous thrombosis in low, medium or high-risk study participants.

"There have been a number of research studies into DVT, and how fliers can counteract the risks," Alison Tierney, the journal's editor-in-chief, said in a prepared statement. "This research review provides a useful overview of some of the most recent comparative research on more than 2,500 fliers, which is why we were so keen to publish it. I personally believe that graduated compression stockings are essential for anyone traveling on long-haul flights," Tierney said.

Living With Deep Vein Thrombosis

Living With Deep Vein Thrombosis

If you've had a deep vein blood clot, you're at greater risk for another one. During treatment and after, it's important to:

Take steps to prevent deep vein thrombosis (DVT). (Search For More information on Google under "How Can Deep Vein Thrombosis Be Prevented?")

Follow these tips:
Check your legs for signs and symptoms of DVT. These include swollen areas, pain or tenderness, increased warmth in swollen or painful areas, or red or discolored skin on the legs.
Contact your doctor right away if you have signs and symptoms of DVT.
Ongoing Health Care Needs

Medicines that thin your blood and prevent blood clots are used to treat DVT. These medicines can thin your blood too much and cause bleeding (sometimes inside the body). This side effect can be life threatening.

Bleeding may occur in the digestive system or the brain. Signs and symptoms of bleeding in the digestive system include:

Bright red vomit or vomit that looks like coffee grounds
Bright red blood in your stools or black, tarry stools
Pain in your abdomen
Signs and symptoms of bleeding in the brain include:

Severe pain in your head
Sudden changes in your vision
Sudden loss of movement in your arms or legs
Memory loss or confusion
If you have any of these signs or symptoms, get treatment right away.

You also should seek treatment right away if you have a lot of bleeding after a fall or injury. This could be a sign that your DVT medicines have thinned your blood too much.

Talk to your doctor before taking any medicines other than your DVT medicines. This includes over-the-counter medicines. Aspirin, for example, also can thin your blood. Taking two medicines that thin your blood may raise your risk for bleeding.

Ask your doctor about how your diet affects these medicines. Foods that contain vitamin K can change how warfarin (a blood-thinning medicine used to treat DVT) works. Vitamin K is found in green, leafy vegetables and some oils, like canola and soybean oil. Your doctor can help you plan a balanced and healthy diet.

Discuss with your doctor whether drinking alcohol will interfere with your medicines. Your doctor can tell you what amount of alcohol is safe for you.

Next Care on Caroline St. - Never Go To Next Care!

Next Care (http://www.nextcare.com/) almost cost me my life.

I went to the Next Care facility located close to Little Five Points in Atlanta, This is the Next Care specifically located in the Edgewood Retail District on Caroline Street (1220 Caroline St., Suite 230, Atlanta, GA 30307). Me and my friends refer to this mammoth shopping center close to L5P as El Grande.

Anyhow, this was the first facility I went to when I thought this blood clot was a leg cramp gone bad. I will not name the doctor at this Next Care emergency clinic on Caroline Street but this quack almost cost me life.

First the receptionist would not take me without my insurance card. Granted it took a lot to walk up the large flight of stairs with a blood clot in my leg ready to kill me at any second but it took even more to have this receptionist tell me that she could not see me until I walked back down the stairs to my car and retrieved my insurance card. I asked the lady nicely if I could get it after the doctor looked at me and the answer was no.

Second after a seemingly meaningless long wait, since I was the only person in there, the doctor saw me. He asked me what I thought the problem was. I told him I thought it was a cramp but my friends were telling me that it could be a blood clot and that I should have it checked out (thanks Ken). The doctor squeezed my leg (one of the worst things you could do since it could force the clot to move) and repeated this "I think it might be a pulled muscle or a blood clot." My mouth gaped open.

I left in shock and called a real doctor. I thought this "Emergency Clinic" would give me some insight into what was going on. They didn't. I was nervous about going to a real doctor because of what they might say but I am telling you don't wait. If you have a twinge of pain or something that feels like a pulled muscle or a leg cramp - get it checked out at a hospital or by your normal physician.

I could have died with the care that was provided by Next Care. Do not use these emergency clinics, they take your money and provide information that is below what you can find yourself on the Internet. Go to a real hospital or doctor if you are sick.

Scuba Diving With DVT

I have been taking a scuba class for the past four days. My good friend thought it would be fun to go scuba diving on a trip we are taking to the Bahamas.

Since then I have been doing a little bit of research on if I can do this activity with the current DVT situation in my leg and with me taking 5mg of Coumodin (aka Warafin) on a daily basis. I guess I should also mention that my doctor has told me that my DVT is more than likely caused from a Vitamin K deficiency and she has suggested that I take this blood thiner for the rest of my life. I am 36 and I find this disturbing so I am researching the idea of trying to replace this warfin with aspirin but thats another post topic.

My NAUI Scuba instructor has some apprehension because he is concerned about the off gassing stage. He came to me the second day of this four day class and told me that I would need to get my doctors approval. The dive store owner at Dive World in Atlanta has a a similar situation but dives anyways (at least thats what the instructor told me). I am going to see my doctor tomorrow and get the official word because the dive instructor wont certify me without a doctors note.

I just finished the dive portion of the class and on the second day of the class we spent a lot of time underwater and did some pretty tricky emergancy manuvers (losing your mask, taking off your BC and recovering it, taking off your weight belt and recovering it, dragging buddies around the pool and simulating mouth to mouth). This was strenuous and the kicking involved was a workout on the leg that had severe blood clots in it just over a year ago.

As I walk around today (after the classes) I am seeing some problems. I am having the same twinges in my legs that I had prior to my blood clot and after a long stint in the hospital. My left leg is also tight in places and I am feeling some of the same leg cramping that I felt when I had my blood clot. Mind you all of these symptoms happened after the second day of diving. I would say with my poor swimming skills that this was a strenuous day of diving activity.

This morning I was also groggy and irritable. I am a black guy (light skinned) and I also noticed that my skin was much darker and a little splotchy.

Anyhow I will post some of the information I found online and will also let you know what the doctor says tomorrow.

I will post under a consistent label to make it easier for the readers of this blog to find other posts.

Today Is DVT Awarness Day

Wow can you believe David Bloom has been gone for 5 years and it took his death to bring DVT to the forefront? Well thanks to him March is DVT awareness month.

His widow Melanie Bloom (prventdvt.org) and his duaghters released a new line of socks to bring attention to the cause.

Check out this link too - http://www.msnbc.msn.com/id/7074940/

Good Information On DVT - Only Taking Coumudin for 1 year

Blood clot in leg vein can be deadly
excerpt taken from Contra Costa Times


Q: Nine months ago, our son, 42, had a deep-vein thrombosis. The clot was in the calf and thigh vein. He was given an anticoagulant and the clot was surgically removed, but surgery was only partly successful. Some of the clot remains in his leg veins. He continues to take Coumadin and is told it may take a year for the clot to dissolve. His calf is often swollen and painful. Can you suggest any additional treatment?

A: For readers unfamiliar with this problem, some definitions are necessary. Thrombophlebitis (THROM-boh-flea-BITE-is) is a clot in a vein. "Thrombo" means "clot," and "phlebitis" is vein inflammation. The leg is the common site for it to happen. A person on bed rest after surgery (especially knee and hip surgery), who is sitting for prolonged times during a car or plane trip, taking birth-control pills or suffering trauma is at risk of getting thrombophlebitis.
Clots in the deep veins of the leg, the ones you cannot see, are the dangerous kind. Bits of those clots can break away from the main clot and be carried in the circulation to the lung, where they can plug a lung blood vessel. That's called a pulmonary embolism, and it can be deadly.
Clots in leg veins cause the overlying skin to turn red and become tender. The leg swells and is painful. Ultrasound examination of the veins establishes the diagnosis.
Anticoagulants are the treatment. They don't dissolve the clot, but they keep it from growing larger and they prevent the chance of a pulmonary embolus. In time, a canal burrows through the clot, and blood flow is re-established or blood finds alternate routes to leave the leg. It takes months for this to occur. Nothing speeds the process. Time is the medicine of choice.
A large number of people develop what's called the post-thrombotic syndrome after thrombophlebitis. The leg remains swollen and painful. Compression stockings and frequent leg elevation minimize this complication.

Coumadin - Forgetting to take coumadin

I have noticed that whenever I forget to take coumadin that I get phantom pains in my leg that the blood clot happened in. Sometimes I get headaches also. I wonder if this has to do with my blood getting thicker???

I have enquired with my doctor about the consequences if I stop taking it and she has told me that it stays in your system for at least three days even though your blood level will gradually get thicker over that time. She smiled and told me that I would feel it if I stopped taking it...

Another nurse told me that one of her patients stopped taking coumadin and kept ending up in the intensive care unit with a heparin bag next to his bed.

These could all be scare tactics to make the drug company who makes coumadin, Bristol-Myers Squibb Company, lots of money. I am very weary of how much influence drug companies have and am always weary of the gift bags I see the drug representatives bring into my doctors office but a little rat poison has never killed anyone right?

My father who had suffered a blood clot that almost killed him, had a doctor that was vehement about him not staying on Bristol-Myers Squibb Companys wonder drug.

All I know is that I can definitely feel some type of twinges of pain in the leg that had the blood clot when I forget to take my coumadin. It usually takes 4 hours but I do feel it.

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.