Tag Archives: Thrombus

Artemisia anomala

Botanical Name :Artemisia anomala
Family :Asteraceae
Genus: Artemisia
Species:A. anomala
Kingdom: Plantae
Order: Asterales

Common Chinese Names :Liu Ji Nu, Qi Hau

Habitat:Artemisia anomala is native to E. AsiaChina. It grows on the forest margins, roadsides, canyons, river banks, shrublands and slopes at levations of 200 – 1200 metres.

Description:
Artemisia anomala is a perennial herb, growing to 1 m (3ft 3in). It is in flower from Jul to November, and the seeds ripen from Aug to November. The flowers are hermaphrodite (have both male and female organs)Suitable for: light (sandy), medium (loamy) and heavy (clay) soils. Suitable pH: acid, neutral and basic (alkaline) soils. It can grow in semi-shade (light woodland) or no shade. It prefers moist soil. CLICK & SEE THE PICTURES
Medicinal Uses:
Used externally in the treatment of burns and inflamed skin. The plant is used for making antiphlogistic and antitoxin drugs. It is very effective for bloating, all types of burnes, indigestion, blood clots. fractures, internal injury, bruises, high blood pressure, menses scanty & ulcers.
Known Hazards: Avoid during pregnancy & breastfeeding. Overdose may cause vomiting & diarrhea.

Disclaimer : The information presented herein is intended for educational purposes only. Individual results may vary, and before using any supplement, it is always advisable to consult with your own health care provi

Resources:
https://vi.wikipedia.org/wiki/Artemisia_anomala
http://herbpathy.com/Uses-and-Benefits-of-Artemisia-Anomala-Cid5102
http://www.pfaf.org/user/Plant.aspx?LatinName=Artemisia+anomala

Blood Clots

Alternative Names: Clot; Emboli; Thrombi

Definition:
Blood is a liquid that flows within blood vessels. It is constantly in motion as the heart pumps blood through arteries to the different organs and cells of the body. The blood is returned back to the heart by the veins. Veins are squeezed when muscles in the body contract and push the blood back to the heart.

Blood clotting is an important mechanism to help the body repair injured blood vessels.

Blood consists of:

•red blood cells containing hemoglobin that carry oxygen to cells and remove carbon dioxide (the waste product of metabolism),

•white blood cells that fight infection,

•platelets that are part of the clotting process of the body, and

•blood plasma, which contains fluid, chemicals and proteins that are important for bodily functions.

Complex mechanisms exist in the bloodstream to form clots where they are needed. If the lining of the blood vessels becomes damaged, platelets are recruited to the injured area to form an initial plug. These activated platelets release chemicals that start the clotting cascade, using a series of clotting factors produced by the body. Ultimately, fibrin is formed, the protein that crosslinks with itself to form a mesh that makes up the final blood clot.

The medical term for a blood clot is a thrombus (plural= thrombi). When a thrombus is formed as part of a normal repair process of the body, there is little consequence. Unfortunately, there are times when a thrombus (blood clot) will form when it is not needed, and this can have potentially significant consequences.
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Thousands more people will have long term health problems as a result of a blood clot in the vein. Many of these people would have been completely unaware that they were at increased risk of venous thrombosis, so missing out on treatment which could be life saving.

Clots can form in any vein deep within the body, but most often can be found in the deep veins of the leg. These deep vein thromboses (DVT) form in the calf or lower leg, behind the knee, in the thigh or in the veins passing through the pelvis.
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Each year more than one in every thousand people in the UK develops a blood clot in a vein, known as a venous thrombosis. For as many as 25,000, the clot will prove fatal; more deaths than from breast cancer, HIV and road traffic accidents combined.

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Causes and risk factors:
There are several factors that significantly increase someone’s risk of developing a venous thrombosis:

•Slowing of blood flow through the veins, for example when someone is confined to bed by illness or to a chair on a long journey.
•Damage to the walls of the blood vessels, for example during surgery on the legs, hips or pelvis, or as a result of age-related changes.
•An increased tendency of the blood to clot, because of inherited problems with the blood’s clotting system, cancer, or the hormone changes of pregnancy (or the contraceptive pill).
You may click to see :Family history linked to increased blood clot risk

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Those particularly at risk include:

•The elderly – one in 100 over the age of 80 are at risk.
•Those who are immobile, because of illness, surgery or travel.
•People undergoing surgery on the hips and knees. More than half of those people having a total hip replacement will develop a DVT if not given preventative medicine.
•Heart attack or stroke patients.
•People with cancer, especially after surgery or if they’re having chemotherapy.
•Women during pregnancy, or if they’re using the contraceptive pill or HRT.
•Those with previous blood clotting problems (including inherited abnormalities of clotting which are much more common than most people realise).
•Smokers.
If the DVT damages the delicate valves which help keep blood flowing upwards towards the heart, a condition called post-phlebitic syndrome may develop (occurring in one in five after a DVT). As a result, blood pools in the lower leg, increasing pressure in the vessels, causing swelling of the leg and ankle and a heavy sensation, especially after walking or standing. Skin ulcers may also develop.
Symptoms:
When the clot forms, it blocks the vein, preventing blood from draining from the limb as it should. The result is that the leg becomes swollen and painful, may change colour (turning pale, blue or reddish-purple) or the skin appears tight or shiny.

More worrying is the risk that part of the clot will break away, forming what is known as an embolus which travels around the circulation, through the heart and into the lungs where it blocks a blood vessel. This is known as a pulmonary embolus (PE) and estimates suggest that as many as 50 per cent of those with a DVT will go on to develop a PE.

The symptoms of PE include chest pain and shortness of breath, which may be sudden and severe. Although some people develop a PE without noticing any symptoms, it can be extremely dangerous and cause damage to the lung tissues proving fatal in as many as one in ten unless treated.

Long term complications include chronic pulmonary hypertension, where the pressure in the blood vessels of the lung remains persistently high.

Possible Complications:
Thrombi and emboli can firmly attach to a blood vessel. They can partially or completely block the flow of blood in that vessel.

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A blockage in the blood vessel prevents normal blood flow and oxygen from reaching the tissues in that location. This is called ischemia. If ischemia is not treated promptly, it can result in tissue damage, or death of the tissues in that area.


Diagnosis
:-
Symptoms of a DVT or PE may be minimal and can often go undiagnosed. When suspected, it can be difficult to reach a definite diagnosis because tests aren’t straightforward and don’t always give a clear result.

Tests include:
•A blood test known as a D-dimer (although a negative result means that a clot is unlikely, a positive can occur in a number of other illnesses so it is not specific for a DVT or PE).
•An ultrasound scan (good for showing a clot behind the knee or in the thigh, but not so accurate for a DVT in the calf). A special type of ultrasound, known as Doppler ultrasound, is increasingly used and can show how fast the blood is flowing through the veins.
•An x-ray dye test known as a venogram (more invasive than ultrasound).
•MRI or CT scans.
•Ventilation/perfusion scan, where the parts of the lung being filled with air are compared with those with blood flowing through them.

Treatment and prevention:
Once a DVT or PE has been diagnosed, treatment is started to thin the blood (known as anticoagulant therapy), reducing the risk that the clot will grow or spread.

Immediate treatment is given in the form of injections of a drug called heparin, and warfarin tablets, which take several days to build effect. When the cause of the clot formation is clear, such as after surgery, treatment is continued for three months, but when there’s no obvious cause it may be continued for six months or even indefinitely.

The effects of warfarin can vary. Other illnesses and treatments, or even a change in diet, can interfere and it’s quite easy to become over – or under – coagulated, leading to a risk of either a haemorrhage or further clots. Those taking warfarin must have regular blood tests to monitor their clotting levels, and the dose of warfarin adjusted accordingly.

Newer drugs are being developed which are more consistent in their effect and which one day may replace warfarin.

When someone is known to be at risk of venous thrombosis, clots can be prevented by taking a few simple steps and giving small doses of anti-coagulant drugs.

Herbal Treatment:-There are certain proven herbal treatments for thrombosis. One of the most prominent herbal treatments for thrombosis is sweet potato. Scientifically it is called Ipomoea batatas. However in the US of A it is popularly known as Yam. This herbal fruit is an antioxidant. It is also abundant in Vitamin A and C.  This being the case it is very effective in treating thrombosis. Another very potent herbal treatment for thrombosis is lemon.  The imbibing of 300 ml of lemon juice for 2 months would lessen the symptoms of thrombosis. These herbal treatments have been tried with success by scores of people with success.

During long distance travel, or other periods of immobility, you should:

•Keep well hydrated
•Wear elastic compression stockings to support blood flow through the veins (it’s important that these are put on correctly)
•Take a little exercise at frequent intervals (if stuck in a seat, carry out simple leg exercises in the chair such as flexing your ankles).
Heparin treatment will reduce the risk of DVT following cancer treatment or hip or knee surgery by 70 per cent. People having major surgery have a 30 per cent risk of DVT which is reduced by about 60 per cent with anti-coagulants.

If you’re going into hospital for an operation or other treatment you should be assessed for your risk of developing a blood clot and in most cases will be offered preventative treatment with anti-coagulant injections. Compression stockings may also be used.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:
http://www.bbc.co.uk/health/physical_health/conditions/bloodclots1.shtml
http://health.nytimes.com/health/guides/disease/deep-venous-thrombosis/overview.html
http://www.mayoclinic.com/health/blood-clots/MY00109/DSECTION=causes
http://www.nlm.nih.gov/medlineplus/ency/article/001124.htm

http://www.herbalgranny.com/2009/08/24/herbal-treatment-for-thrombosis/

Poor Immune System and Low Levels of Antibodies Linked to Stroke

A study shows that the chances of suffering a stroke are linked to the presence of a certain type of antibody in the immune system.

click  to see the pictures

The research group, which was led by Professor Johan Frostegård, has previously demonstrated that high levels of a certain type of antibody (anti-PC) in the immune defense are linked to a reduced risk of arteriosclerosis, a common cause of thrombosis and myocardial infarction.

In the present study, the researchers focused exclusively on stroke – a blood clot in the brain – and compared 227 individuals who had suffered stroke over a 13-year period with 445 sex and age-matched controls. After controlling for other risk factors (age, sex, smoking habits, cholesterol levels, diabetes, BMI and blood pressure), they were able to show that low levels (below 30 per cent of average) of PC antibodies correlated with a higher risk of stroke, which in women meant an almost three-fold increase.

The researchers have now advanced the hypothesis that low levels of natural PC antibodies, which can be a condition of a poor immune system – contribute to the development of arteriosclerosis and its consequences, which include stroke.

Arteriosclerosis is formed by the accumulation of plaque on the walls of blood vessels, which can rupture and form a blood clot. The researchers believe that the PC antibodies react to a substance called phosphorylcholine (PC), which is a component of a class of fat molecules (phospholipids) that go to make up the plaque.

Source: Elements4Health

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Pulmonary Embolism

Definition:-
Pulmonary embolism (PE) is a blockage of the main artery of the lung or one of its branches by a substance that has travelled from elsewhere in the body through the bloodstream (embolism). Usually this is due to embolism of a thrombus (blood clot) from the deep veins in the legs, a process termed venous thromboembolism. A small proportion is due to the embolization of air, fat or amniotic fluid. The obstruction of the blood flow through the lungs and the resultant pressure on the right ventricle of the heart leads to the symptoms and signs of PE. The risk of PE is increased in various situations, such as cancer and prolonged bed rest..

You may click to see more pictures of Pulmonary Embolism
Pulmonary embolism is a condition that occurs when one or more arteries in your lungs become blocked. In most cases, pulmonary embolism is caused by blood clots that travel to your lungs from another part of your body — most commonly, your legs.

Symptoms:-
Symptoms of PE are sudden-onset dyspnea (shortness of breath), tachypnea (rapid breathing), chest pain of a “pleuritic” nature (worsened by breathing), cough and hemoptysis (coughing up blood). More severe cases can include signs such as cyanosis (blue discoloration, usually of the lips and fingers), collapse, and circulatory instability. About 15% of all cases of sudden death are attributable to PE.

On physical examination, a pleural rub may be audible by stethoscope over affected areas of the lung. Strain on the right ventricle may be detected as a left parasternal heave, a loud pulmonary component of the second heart sound, raised jugular venous pressure, and more rarely leg swelling.

A fever though usually low grade is present in 14% of people with pulmonary embolism.

Symptoms of pulmonary embolism include difficulty breathing, chest pain on inspiration, and palpitations. Clinical signs include low blood oxygen saturation and cyanosis, rapid breathing, and a rapid heart rate. Severe cases of PE can lead to collapse, abnormally low blood pressure, and sudden death.

Pulmonary embolism occurs when a clump of material, most often a blood clot, gets wedged into an artery in your lungs. These blood clots most commonly originate in the deep veins of your legs, but they can also come from other parts of your body. This condition is known as deep vein thrombosis (DVT).

Occasionally, other substances can form blockages within the blood vessels inside your lungs. Examples include:

*Fat from within the marrow of a broken bone
*Part of a tumor
*Air bubbles

It’s rare to experience a solitary pulmonary embolism. In most cases, multiple clots are involved. The lung tissue served by each blocked artery is robbed of fuel and may die. This makes it more difficult for your lungs to provide oxygen to the rest of your body.

Because pulmonary embolism almost always occurs in conjunction with deep vein thrombosis, some doctors refer to the two conditions together as venous thromboembolism (VTE).

Causes:-

In 9 out of 10 cases, pulmonary embolism (PE) begins as a blood clot in the deep veins of the leg (a condition known as deep vein thrombosis). The clot breaks free from the vein and travels through the bloodstream to the lungs, where it can block an artery.Click to see to learn more

Diagnosis:-
The diagnosis of PE is based primarily on validated clinical criteria combined with selective testing because the typical clinical presentation (shortness of breath, chest pain) cannot be definitively differentiated from other causes of chest pain and shortness of breath. The decision to do medical imaging is usually based on clinical grounds, i.e. the medical history, symptoms and findings on physical examination, followed by an assessment of clinical probability.

The most commonly used method to predict clinical probability, the Wells score, is a clinical prediction rule, whose use is complicated by multiple versions being available. In 1995, Wells et al. initially developed a prediction rule (based on a literature search) to predict the likelihood of PE, based on clinical criteria. The prediction rule was revised in 1998 This prediction rule was further revised when simplified during a validation by Wells et al. in 2000. In the 2000 publication, Wells proposed two different scoring systems using cutoffs of 2 or 4 with the same prediction rule. In 2001, Wells published results using the more conservative cutoff of 2 to create three categories. An additional version, the “modified extended version”, using the more recent cutoff of 2 but including findings from Wells’s initial studies were proposed. Most recently, a further study reverted to Wells’s earlier use of a cutoff of 4 points to create only two categories.

There are additional prediction rules for PE, such as the Geneva rule. More importantly, the use of any rule is associated with reduction in recurrent thromboembolism.

The Wells score:
*Clinically suspected DVT – 3.0 points
*Alternative diagnosis is less likely than PE – 3.0 points
*Tachycardia – 1.5 points
*Immobilization/surgery in previous four weeks – 1.5 points
*History of DVT or PE – 1.5 points
*Hemoptysis – 1.0 points
*Malignancy (treatment for within 6 months, palliative) – 1.0 points

Traditional interpretation

*Score >6.0 – High (probability 59% based on pooled data)
*Score 2.0 to 6.0 – Moderate (probability 29% based on pooled data)
*Score <2.0 – Low (probability 15% based on pooled data)

Alternate interpretation.
:-
*Score > 4 – PE likely. Consider diagnostic imaging.
*Score 4 or less – PE unlikely. Consider D-dimer to rule out PE.

Blood tests:-
In low/moderate suspicion of PE, a normal D-dimer level (shown in a blood test) is enough to exclude the possibility of thrombotic PE.

When a PE is being suspected, a number of blood tests are done, in order to exclude important secondary causes of PE. This includes a full blood count, clotting status (PT, APTT, TT), and some screening tests (erythrocyte sedimentation rate, renal function, liver enzymes, electrolytes). If one of these is abnormal, further investigations might be warranted.

Non-invasive imaging:-
CT pulmonary angiography (CTPA) is a pulmonary angiogram obtained using computed tomography (CT) with radiocontrast rather than right heart catheterization. Its advantages are clinical equivalence, its non-invasive nature, its greater availability to patients, and the possibility of identifying other lung disorders from the differential diagnosis in case there is no pulmonary embolism. Assessing the accuracy of CT pulmonary angiography is hindered by the rapid changes in the number of rows of detectors available in multidetector CT (MDCT) machines.[14] A study with a mixture of 4 slice and 16 slice scanners reported a sensitivity of 83% and a specificity of 96%. This study noted that additional testing is necessary when the clinical probability is inconsistent with the imaging results.[15] CTPA is non-inferior to VQ scanning, and identifies more emboli (without necessarily improving the outcome) compared to VQ scanning

Ventilation/perfusion scan (or V/Q scan or lung scintigraphy), which shows that some areas of the lung are being ventilated but not perfused with blood (due to obstruction by a clot). This type of examination is used less often because of the more widespread availability of CT technology, however, it may be useful in patients who have an allergy to iodinated contrast or in pregnancy due to lower radiation exposure than CT

Ventilation/perfusion scan (or V/Q scan or lung scintigraphy), which shows that some areas of the lung are being ventilated but not perfused with blood (due to obstruction by a clot). This type of examination is used less often because of the more widespread availability of CT technology, however, it may be useful in patients who have an allergy to iodinated contrast or in pregnancy due to lower radiation exposure than CT.

Low probability diagnostic tests/non-diagnostic tests:-

Tests that are frequently done that are not sensitive for PE, but can be diagnostic.

*Chest X-rays are often done on patients with shortness of breath to help rule-out other causes, such as congestive heart failure and rib fracture. Chest X-rays in PE are rarely normal,[18] but usually lack signs that suggest the diagnosis of PE (e.g. Westermark sign, Hampton’s hump).

*Ultrasonography of the legs, also known as leg doppler, in search of deep venous thrombosis (DVT). The presence of DVT, as shown on ultrasonography of the legs, is in itself enough to warrant anticoagulation, without requiring the V/Q or spiral CT scans (because of the strong association between DVT and PE). This may be valid approach in pregnancy, in which the other modalities would increase the risk of birth defects in the unborn child. However, a negative scan does not rule out PE, and low-radiation dose scanning may be required if the mother is deemed at high risk of having pulmonary embolism.

Electrocardiogram findings:-
Electrocardiogram of a patient with pulmonary embolism showing sinus tachycardia of approximately 150 beats per minute and right bundle branch block.An electrocardiogram (ECG) is routinely done on patients with chest pain to quickly diagnose myocardial infarctions (heart attacks). An ECG may show signs of right heart strain or acute cor pulmonale in cases of large PEs – the classic signs are a large S wave in lead I, a large Q wave in lead III and an inverted T wave in lead III (“S1Q3T3”). This is occasionally (up to 20%) present, but may also occur in other acute lung conditions and has therefore limited diagnostic value. The most commonly seen signs in the ECG is sinus tachycardia, right axis deviation and right bundle branch block. Sinus tachycardia was however still only found in 8 – 69% of people with PE.

Echocardiography findings:-
In massive and submassive PE, dysfunction of the right side of the heart can be seen on echocardiography, an indication that the pulmonary artery is severely obstructed and the heart is unable to match the pressure. Some studies  suggest that this finding may be an indication for thrombolysis. Not every patient with a (suspected) pulmonary embolism requires an echocardiogram, but elevations in cardiac troponins or brain natriuretic peptide may indicate heart strain and warrant an echocardiogram.

The specific appearance of the right ventricle on echocardiography is referred to as the McConnell sign. This is the finding of akinesia of the mid-free wall but normal motion of the apex. This phenomenon has a 77% sensitivity and a 94% specificity for the diagnosis of acute pulmonary embolism.

Combining tests into algorithms:-
Recent recommendations for a diagnostic algorithm have been published by the PIOPED investigators; however, these recommendations do not reflect research using 64 slice MDCT.[12] These investigators recommended:

*Low clinical probability. If negative D-dimer, PE is excluded. If positive D-dimer, obtain MDCT and based treatment on results.

*Moderate clinical probability. If negative D-dimer, PE is excluded. However, the authors were not concerned that a negative MDCT with negative D-dimer in this setting has an 5% probability of being false. Presumably, the 5% error rate will fall as 64 slice MDCT is more commonly used. If positive D-dimer, obtain MDCT and based treatment on results.

*High clinical probability. Proceed to MDCT. If positive, treat, if negative, additional tests are needed to exclude PE.

Pulmonary Embolism Rule-out Criteria:-
The Pulmonary Embolism Rule-out Criteria, or PERC rule, helps assess patients in whom pulmonary embolism is suspected, but unlikely. Unlike the Wells Score and Geneva score, which are clinical prediction rules intended to risk stratify patients with suspected PE, the PERC rule is designed to rule-out risk of PE in patients when the physician has already stratified them into a low-risk category.

Patients in this low risk category without any of these criteria may undergo no further diagnostic testing for PE: Hypoxia – Sa02 <95%, unilateral leg swelling, hemoptysis, prior DVT or PE, recent surgery or trauma, age >50, hormone use, tachycardia. The rationale behind this decision is that further testing (specifically CT angiogram of the chest) may cause more harm (from radiation exposure and contrast dye) than the risk of PE.[24] The PERC rule has a sensitivity of 97.4% and specificity of 21.9% with a false negative rate of 1.0% (16/1666).

Treatment:-
In most cases, anticoagulant therapy is the mainstay of treatment. Acutely, supportive treatments, such as oxygen or analgesia, are often required.

Anticoagulation:-
In most cases, anticoagulant therapy is the mainstay of treatment. Heparin, low molecular weight heparins (such as enoxaparin and dalteparin), or fondaparinux is administered initially, while warfarin, acenocoumarol, or phenprocoumon therapy is commenced (this may take several days, usually while the patient is in hospital). It however may be possible to treat low risk patients as outpatients. An ongoing study is looking into the safety of this practice. Warfarin therapy often requires frequent dose adjustment and monitoring of the INR. In PE, INRs between 2.0 and 3.0 are generally considered ideal. If another episode of PE occurs under warfarin treatment, the INR window may be increased to e.g. 2.5-3.5 (unless there are contraindications) or anticoagulation may be changed to a different anticoagulant e.g. low molecular weight heparin. In patients with an underlying malignancy, therapy with a course of low molecular weight heparin may be favored over warfarin based on the results of the CLOT trial. Similarly, pregnant women are often maintained on low molecular weight heparin to avoid the known teratogenic effects of warfarin, especially in the early stages of pregnancy. People are usually admitted to hospital in the early stages of treatment, and tend to remain under inpatient care until INR has reached therapeutic levels. Increasingly, low-risk cases are managed on an outpatient basis in a fashion already common in the treatment of DVT.

Warfarin therapy is usually continued for 3–6 months, or “lifelong” if there have been previous DVTs or PEs, or none of the usual risk factors is present. An abnormal D-dimer level at the end of treatment might signal the need for continued treatment among patients with a first unprovoked pulmonary embolus.

Thrombolysis:-
Massive PE causing hemodynamic instability (shock and/or hypotension, defined as a systolic blood pressure <90 mmHg or a pressure drop of 40 mmHg for>15 min if not caused by new-onset arrhythmia, hypovolemia or sepsis) is an indication for thrombolysis, the enzymatic destruction of the clot with medication. It is the best available medical treatment in this situation and is supported by clinical guidelines.

The use of thrombolysis in non-massive PEs is still debated. The aim of the therapy is to dissolve the clot, but there is an attendant risk of bleeding or stroke. The main indication for thrombolysis is in submassive PE where right ventricular dysfunction can be demonstrated on echocardiography, and the presence of visible thrombus in the atrium.

Surgical management:-
Surgical management of acute pulmonary embolism (pulmonary thrombectomy) is uncommon and has largely been abandoned because of poor long-term outcomes. However, recently, it has gone through a resurgence with the revision of the surgical technique and is thought to benefit selected patients

Chronic pulmonary embolism leading to pulmonary hypertension (known as chronic thromboembolic hypertension) is treated with a surgical procedure known as a pulmonary thromboendarterectomy.

Inferior vena cava filter:-
If anticoagulant therapy is contraindicated and/or ineffective, or to prevent new emboli from entering the pulmonary artery and combining with an existing blockage, an inferior vena cava filter may be implanted.

Prognosis:-
Mortality from untreated PE is said to be 26%. This figure comes from a trial published in 1960 by Barrit and Jordan,[38] which compared anticoagulation against placebo for the management of PE. Barritt and Jordan performed their study in the Bristol Royal Infirmary in 1957. This study is the only placebo controlled trial ever to examine the place of anticoagulants in the treatment of PE, the results of which were so convincing that the trial has never been repeated as to do so would be considered unethical. That said, the reported mortality rate of 26% in the placebo group is probably an overstatement, given that the technology of the day may have detected only severe PEs.

Prognosis depends on the amount of lung that is affected and on the co-existence of other medical conditions; chronic embolisation to the lung can lead to pulmonary hypertension. After a massive PE, the embolus must be resolved somehow if the patient is to survive. In thrombotic PE, the blood clot may be broken down by fibrinolysis, or it may be organized and recanalized so that a new channel forms through the clot. Blood flow is restored most rapidly in the first day or two after a PE. Improvement slows thereafter, and some defects may remain permanently. There is controversy over whether or not small subsegmental PEs need to be treated at all[40] and some evidence exists that patients with subsegmental PEs may do well without treatment.

Predicting mortality:-
The PESI and Geneva prediction rules can estimate mortality and so may guide selection of patients who can be considered for outpatient therapy.

Underlying causes:-
After a first PE, the search for secondary causes is usually brief. Only when a second PE occurs, and especially when this happens while still under anticoagulant therapy, a further search for underlying conditions is undertaken. This will include testing (“thrombophilia screen”) for Factor V Leiden mutation, antiphospholipid antibodies, protein C and S and antithrombin levels, and later prothrombin mutation, MTHFR mutation, Factor VIII concentration and rarer inherited coagulation abnormalities.

Epidemiology:-

Risk factors:-
The most common sources of embolism are proximal leg deep venous thrombosis (DVTs) or pelvic vein thromboses. Any risk factor for DVT also increases the risk that the venous clot will dislodge and migrate to the lung circulation, which happens in up to 15% of all DVTs. The conditions are generally regarded as a continuum termed venous thromboembolism (VTE).

The development of thrombosis is classically due to a group of causes named Virchow’s triad (alterations in blood flow, factors in the vessel wall and factors affecting the properties of the blood). Often, more than one risk factor is present.

*Alterations in blood flow: immobilization (after surgery, injury or long-distance air travel), pregnancy (also procoagulant), obesity (also procoagulant)

*Factors in the vessel wall: of limited direct relevance in VTE

*Factors affecting the properties of the blood (procoagulant state):

*Oestrogen-containing hormonal contraception
*Genetic thrombophilia (factor V Leiden, prothrombin mutation G20210A, protein C deficiency, protein S deficiency, antithrombin deficiency, hyperhomocysteinemia and plasminogen/fibrinolysis disorders).
*Acquired thrombophilia (antiphospholipid syndrome, nephrotic syndrome, paroxysmal nocturnal hemoglobinuria)

Prognosis:-
Once anticoagulation is stopped, the risk of a fatal pulmonary embolism is 0.5% per year

Prevention:-
If you are in hospital for surgery or because of illness, your doctor will suggest some leg exercises you can do, to ensure you keep your legs moving. You will be encouraged to drink plenty of fluids (or may have fluids via a drip if you are unable to drink).

If you are having major surgery, you may be given injections of heparin before your surgery to reduce your risk of getting a DVT or pulmonary embolism. You may also be given elastic compression stockings to wear or a device called an intermittent compression pump to keep the blood flowing through your legs.

*Compression stockings (also called TED or thrombo-embolic deterrent stockings) are usually worn to help maintain circulation and reduce the risk of blood clots forming in the veins of your legs. They come in different sizes and will be checked by nursing staff every day to make sure that they’re the correct size and fit for you. You might be asked to wear them after you have had surgery.

*Intermittent compression pumps help to dissolve blood clots by compressing the calf and/or thigh muscles of your leg. They are usually used straight before or during surgery.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:-
http://www.betterhealthresearch.com/news/researchers-may-have-found-an-efficient-way-to-detect-pulmonary-embolisms-19522007/
http://en.wikipedia.org/wiki/Pulmonary_embolism
http://www.mayoclinic.com/health/pulmonary-embolism/DS00429/DSECTION=causes

http://hcd2.bupa.co.uk/fact_sheets/html/Pulmonary_embolism.html

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Coming soon, the Hips and Knees that will Never Wear Out

Replacement body parts that never wear out could become a reality within a few years as the  scientists say.

Dodgy knees and hips will be repaired using tissue engineering, while donor heart valves from animals are being specially treated to last indefinitely.
Longer-lasting artificial joints are already being tested in a bid to ensure people will be able to enjoy another 50 active years.

click & see
X-ray of female pelvix with total hips replacement

Scientists at the University of Leeds Institute of Medical and Biological Engineering have launched a £50million research initiative focused on areas of the body most affected by ageing, including joints, spine, teeth, heart and circulation.

Unlike studies involving stem cells and growing ‘spare parts’ in a lab, the programme uses the body’s own regenerative systems. The Leeds scientists have developed a chemical wash that strips cells away from donated cartilage, heart valves, blood vessels and other tissue before they are put into a human body.
Research shows they become repopulated with cells within about six months. Some 40 patients have already been treated with modified heart valves in a study in Brazil.

Professor John Fisher, director of the institute and one of the world’s leading researchers into artificial joints, said research so far had shown the valves did not deteriorate and were not rejected by the body, because ‘foreign’ donor cells had all been stripped away.
The unique method of removing living cells from human and animal tissue creates a biological ‘scaffold’ that can be regenerated within the body, at the site which needs repairing.

Worn-out ligaments and cartilage in knees can be replaced with a scaffold that will eventually attract cells to make the joint last longer.

Other areas targeted for treatment are the spine  –  where discs can be replaced  –  elbow and shoulder tissues and parts of the knee. Vascular patches are being devised that seal the holes made in arteries when surgeons clear a blockage.

The technique is not suitjointsable for whole organs, however. Professor Fisher has also designed a ceramic-on-metal hip joint that reduces ten-fold the wear and tear on artificial joints.

As a result people should be able to get spare parts at an earlier age, when they are less disabled, and they could last up to 50 years, he said.

The professor added: ‘Hip have been used for nearly 50 years but nowadays people want to cycle, play tennis, even go skiing, so they have to last longer.’
He said a scaffolding transplant would cost only around &pound;1,000 a time. It was much more expensive to grow cells outside the body, and there was a higher infection risk.

Professor Eileen Ingham, deputy director of the Institute, said stem cells were not the answer to structural replacement of wornout bits of the body such as heart valves.

She said: ‘We are working with the NHS National Blood & Transplant Tissue Services to apply it to human donor valves. Once a patient has one, it should last a lifetime.’

Professor Christina Doyle, chief executive of Xeno Medical, predicted that in 20-30 years there would be techniques capable of regenerating human tissue off-the-shelf for use in operations.

She said: ‘It will be a case of the surgeon dialling up for spare parts to be delivered in a sterilised plastic bag.’

Source:Mail Online, 20th. Oct.’09

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