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Complications In Pregnancy

 

Pre-eclampsia, eclampsia or toxemia of pregnancy
Definition:
Pre-eclampsia or preeclampsia (PE) is a disorder of pregnancy characterized by high blood pressure and a large amount of protein in the urine. The disorder usually occurs in the third trimester of pregnancy and gets worse over time. In severe disease there may be red blood cell breakdown, a low blood platelet count, impaired liver function, kidney dysfunction, swelling, shortness of breath due to fluid in the lungs, or visual disturbances. PE increases the risk of poor outcomes for both the mother and the baby. If left untreated, it may result in seizures at which point it is known as eclampsia.

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Toxemia of pregnancy is a severe condition that sometimes occurs in the latter weeks of pregnancy. It is characterized by high blood pressure; swelling of the hands, feet, and face; and an excessive amount of protein in the urine. If the condition is allowed to worsen, the mother may experience convulsions and coma, and the baby may be stillborn.
The term toxemia is actually a misnomer from the days when it was thought that the condition was caused by toxic (poisonous) substances in the blood. The illness is more accurately called preeclampsia before the convulsive stage and eclampsia afterward.

Preeclampsia affects between 2–8% of pregnancies worldwide. Hypertensive disorders of pregnancy are one of the most common causes of death due to pregnancy. They resulted in 29,000 deaths in 2013 – down from 37,000 deaths in 1990. Preeclampsia usually occurs after 32 weeks; however, if it occurs earlier it is associated with worse outcomes. Women who have had PE are at increased risk of heart disease later in life. The word eclampsia is from the Greek term for lightning. The first known description of the condition was by Hippocrates in the 5th century BCE

Symptoms:
Swelling (especially in the hands and face) was originally considered an important sign for a diagnosis of preeclampsia. However, because swelling is a common occurrence in pregnancy, its utility as a distinguishing factor in preeclampsia is not great. Pitting edema (unusual swelling, particularly of the hands, feet, or face, notable by leaving an indentation when pressed on) can be significant, and should be reported to a health care provider.

In general, none of the signs of preeclampsia are specific, and even convulsions in pregnancy are more likely to have causes other than eclampsia in modern practice. Further, a symptom such as epigastric pain may be misinterpreted as heartburn. Diagnosis, therefore, depends on finding a coincidence of several preeclamptic features, the final proof being their regression after delivery.

The symptoms of toxemia of pregnancy (which may lead to death if not treated) are divided into three stages, each progressively more serious:
Mild preeclampsia symptoms include edema (puffiness under the skin due to fluid accumulation in the body tissues, often noted around the ankles), mild elevation of blood pressure, and the presence of small amounts of protein in the urine.

Severe preeclampsia symptoms include extreme edema, extreme elevation of blood pressure, the presence of large amounts of protein in the urine, headache, dizziness, double vision, nausea, vomiting, and severe pain in the right upper portion of the abdomen.
Eclampsia symptoms include convulsions and coma.

Risk Factors:
Known risk factors for preeclampsia include:

*Nulliparity (never given birth)
*Older age, and diabetes mellitus
*Kidney disease
*Chronic hypertension
*Prior history of preeclampsia
*Family history of preeclampsia
*Advanced maternal age (>35 years)
*Obesity
*Antiphospholipid antibody syndrome
*Multiple gestation
*Having donated a kidney.
*Having sub-clinical hypothyroidism or thyroid antibodies

It is also more frequent in a women’s first pregnancy and if she is carrying twins. The underlying mechanism involves abnormal formation of blood vessels in the placenta amongst other factors. Most cases are diagnosed before delivery. Rarely, preeclampsia may begin in the period after delivery. While historically both high blood pressure and protein in the urine were required to make the diagnosis, some definitions also include those with hypertension and any associated organ dysfunction. Blood pressure is defined as high when it is greater than 140 mmHg systolic or 90 mmHg diastolic at two separate times, more than four hours apart in a women after twenty weeks of pregnancy. PE is routinely screened for during prenatal care.
Causes:
There is no definitive known cause of preeclampsia, though it is likely related to a number of factors. Some of these factors include:

*Abnormal placentation (formation and development of the placenta)
*Immunologic factors
*Prior or existing maternal pathology – preeclampsia is seen more at a higher incidence in individuals with preexisting hypertension, obesity, antiphospholipid antibody syndrome, and those with history of preeclampsia
*Dietary factors, e.g. calcium supplementation in areas where dietary calcium intake is low has been shown to reduce the risk of preeclampsia.
*Environmental factors, e.g. air pollution
*Those with long term high blood pressure have a risk 7 to 8 times higher than those without.

Physiologically, research has linked preeclampsia to the following physiologic changes: alterations in the interaction between the maternal immune response and the placenta, placental injury, endothelial cell injury, altered vascular reactivity, oxidative stress, imbalance among vasoactive substances, decreased intravascular volume, and disseminated intravascular coagulation.

While the exact cause of preeclampsia remains unclear, there is strong evidence that a major cause predisposing a susceptible woman to preeclampsia is an abnormally implanted placenta. This abnormally implanted placenta is thought to result in poor uterine and placental perfusion, yielding a state of hypoxia and increased oxidative stress and the release of anti-angiogenic proteins into the maternal plasma along with inflammatory mediators. A major consequence of this sequence of events is generalized endothelial dysfunction. The abnormal implantation is thought to stem from the maternal immune system’s response to the placenta and refers to evidence suggesting a lack of established immunological tolerance in pregnancy. Endothelial dysfunction results in hypertension and many of the other symptoms and complications associated with preclampsia.

One theory proposes that certain dietary deficiencies may be the cause of some cases. Also, there is the possibility that some forms of preeclampsia and eclampsia are the result of deficiency of blood flow in the uterus.

Diagnosis:
Pre-eclampsia is diagnosed when a pregnant woman develops:

*Blood pressure >_ 140 mm Hg systolic or  >_  90 mm Hg diastolic on two separate readings taken at least four to six hours apart after 20 weeks gestation in an individual with previously normal blood pressure.
*In a woman with essential hypertension beginning before 20 weeks gestational age, the diagnostic criteria are: an increase in systolic blood pressure (SBP) of   >_ 30mmHg or an increase in diastolic blood pressure (DBP) of   >_15mmHg.
*Proteinuria  >_ 0.3 grams (300 mg) or more of protein in a 24-hour urine sample or a SPOT urinary protein to creatinine ratio  >_ 0.3 or a urine dipstick reading of 1+ or greater (dipstick reading should only be used if other quantitative methods are not available)

Suspicion for preeclampsia should be maintained in any pregnancy complicated by elevated blood pressure, even in the absence of proteinuria. Ten percent of individuals with other signs and symptoms of preeclampsia and 20% of individuals diagnosed with eclampsia show no evidence of proteinuria. In the absence of proteinuria, the presence of new-onset hypertension (elevated blood pressure) and the new onset of one or more of the following is suggestive of the diagnosis of preeclampsia:

*Evidence of kidney dysfunction (oliguria, elevated creatinine levels)
*Impaired liver function (impaired liver function tests)
*Thrombocytopenia (platelet count <100,000/microliter)
*Pulmonary edema
*Ankle edema pitting type
*Cerebral or visual disturbances
*Preeclampsia is a progressive disorder and these signs of organ dysfunction are indicative of severe preeclampsia. A systolic blood pressure ?160 or diastolic blood pressure ?110 and/or proteinuria >5g in a 24-hour period is also indicative of severe preeclampsia. Clinically, individuals with severe preeclampsia may also present epigastric/right upper quadrant abdominal pain, headaches, and vomiting. Severe preeclampsia is a significant risk factor for intrauterine fetal death.

Of note, a rise in baseline blood pressure (BP) of 30 mmHg systolic or 15 mmHg diastolic, while not meeting the absolute criteria of 140/90, is still considered important to note, but is not considered diagnostic.

Predictive tests:
There have been many assessments of tests aimed at predicting preeclampsia, though no single biomarker is likely to be sufficiently predictive of the disorder. Predictive tests that have been assessed include those related to placental perfusion, vascular resistance, kidney dysfunction, endothelial dysfunction, and oxidative stress. Examples of notable tests include:

*Doppler ultrasonography of the uterine arteries to investigate for signs of inadequate placental perfusion. This test has a high negative predictive value among those individuals with a history of prior preeclampsia.
*Elevations in serum uric acid (hyperuricemia) is used by some to “define” preeclampsia,[14] though it has been found to be a poor predictor of the disorder. Elevated levels in the blood (hyperuricemia) are likely due to reduced uric acid clearance secondary to impaired kidney function.
*Angiogenic proteins such as vascular endothelial growth factor (VEGF) and placental growth factor (PIGF) and anti-angiogenic proteins such as soluble fms-like tyrosine kinase-1 (sFlt-1) have shown promise for potential clinical use in diagnosing preeclampsia, though evidence is sufficient to recommend a clinical use for these markers.
*Recent studies have shown that looking for podocytes, specialized cells of the kidney, in the urine has the potential to aid in the prediction of preeclampsia. Studies have demonstrated that finding podocytes in the urine may serve as an early marker of and diagnostic test for preeclampsia. Research is ongoing.

Differential diagnosis:
Pre-eclampsia can mimic and be confused with many other diseases, including chronic hypertension, chronic renal disease, primary seizure disorders, gallbladder and pancreatic disease, immune or thrombotic thrombocytopenic purpura, antiphospholipid syndrome and hemolytic-uremic syndrome. It must be considered a possibility in any pregnant woman beyond 20 weeks of gestation. It is particularly difficult to diagnose when preexisting disease such as hypertension is present. Women with acute fatty liver of pregnancy may also present with elevated blood pressure and protein in the urine, but differs by the extent of liver damage. Other disorders that can cause high blood pressure include thyrotoxicosis, pheochromocytoma, and drug misuse
Treatment:
Preeclampsia and eclampsia cannot be completely cured until the pregnancy is over. Until that time, treatment includes the control of high blood pressure and the intravenous administration of drugs to prevent convulsions. Drugs may also be given to stimulate the production of urine. In some severe cases, early delivery of the baby is needed to ensure the survival of the mother.

Prevention:
Recommendations for prevention include: aspirin in those at high risk, calcium supplementation in areas with low intake, and treatment of prior hypertension with medications. In those with PE delivery of the fetus and placenta is an effective treatment. When delivery becomes recommended depends on how severe the PE and how far along in pregnancy a person is. Blood pressure medication, such as labetalol and methyldopa, may be used to improve the mother’s condition before delivery. Magnesium sulfate may be used to prevent eclampsia in those with severe disease. Bedrest and salt intake have not been found to be useful for either treatment or prevention.

Diet:
Protein or calorie supplementation have no effect on preeclampsia rates, and dietary protein restriction does not appear to increase preeclampsia rates. Further, there is no evidence that changing salt intake has an effect.

Supplementation with antioxidants such as vitamin C and E has no effect on preeclampsia incidence, nor does supplementation with vitamin D. Therefore, supplementation with vitamins C, E, and D is not recommended for reducing the risk of pre-eclampsia.

Calcium supplementation of at least 1 gram per day is recommended during pregnancy as it prevents preeclampsia where dietary calcium intake is low, especially for those at high risk. Low selenium status is associated with higher incidence of preeclampsia.

Aspirin:
Taking aspirin is associated with a 1% to 5% reduction in preeclampsia and a 1% to 5% reduction in premature births in women at high risk. The WHO recommends low-dose aspirin for the prevention of preeclampsia in women at high risk and recommend it be started before 20 weeks of pregnancy. The United States Preventive Services Task Force recommends a low-dose regimen for women at high risk beginning in the 12th week.

Physical activity:
There is insufficient evidence to recommend either exercise or strict bedrest as preventative measures of pre-eclampsia.

Smoking cessation:
In low-risk pregnancies the association between cigarette smoking and a reduced risk of preeclampsia has been consistent and reproducible across epidemiologic studies. High-risk pregnancies (those with pregestational diabetes, chronic hypertension, history of preeclampsia in a previous pregnancy, or multifetal gestation) showed no significant protective effect. The reason for this discrepancy is not definitively known; research supports speculation that the underlying pathology increases the risk of preeclampsia to such a degree that any measurable reduction of risk due to smoking is masked. However, the damaging effects of smoking on overall health and pregnancy outcomes outweighs the benefits in decreasing the incidence of preeclampsia. It is recommended that smoking be stopped prior to, during and after pregnancy

Restriction of salt in the diet may help reduce swelling, it does not prevent the onset of high blood pressure or the appearance of protein in the urine. During prenatal visits, the doctor routinely checks the woman’s weight, blood pressure, and urine. If toxemia is detected early, complications may be reduced.

Resources:
http://health.howstuffworks.com/pregnancy-and-parenting/pregnancy/complications/a-guide-to-pregnancy-complications-ga13.htm
http://en.wikipedia.org/wiki/Pre-eclampsia

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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
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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/

Atrial Fibrillation

Definition:
Atrial fibrillation (AF or A-fib) is the most common cardiac arrhythmia (abnormal heart rhythm) and involves the two upper chambers (atria) of the heart. Its name comes from the fibrillating (i.e. quivering) of the heart muscles of the atria, instead of a coordinated contraction. It can often be identified by taking a pulse and observing that the heartbeats don’t occur at regular intervals. However, a stronger indicator of AF is the absence of P waves on an electrocardiogram (ECG or EKG), which are normally present when there is a coordinated atrial contraction at the beginning of each heart beat. Risk increases with age, with 8% of people over 80 having AF.

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In AF, the normal electrical impulses that are generated by the sinoatrial node are overwhelmed by disorganized electrical impulses that originate in the atria and pulmonary veins, leading to conduction of irregular impulses to the ventricles that generate the heartbeat. The result is an irregular heartbeat which may occur in episodes lasting from minutes to weeks, or it could occur all the time for years. The natural tendency of AF is to become a chronic condition. Chronic AF leads to a small increase in the risk of death.

Atrial fibrillation is often asymptomatic, and is not in itself generally life-threatening, but may result in palpitations, fainting, chest pain, or congestive heart failure. People with AF usually have a significantly increased risk of stroke (up to 7 times that of the general population). Stroke risk increases during AF because blood may pool and form clots in the poorly contracting atria and especially in the left atrial appendage (LAA).[4] The level of increased risk of stroke depends on the number of additional risk factors. If a person with AF has none, the risk of stroke is similar to that of the general population. However, many people with AF do have additional risk factors and AF is a leading cause of stroke.

Atrial fibrillation may be treated with medications which either slow the heart rate or revert the heart rhythm back to normal. Synchronized electrical cardioversion may also be used to convert AF to a normal heart rhythm. Surgical and catheter-based therapies may also be used to prevent recurrence of AF in certain individuals. People with AF are often given anticoagulants such as warfarin to protect them from stroke.

Classification: The American College of Cardiology (ACC), American Heart Association (AHA), and the European Society of Cardiology (ESC) recommend in their guidelines the following classification system based on simplicity and clinical relevance.

AF Category…………… Defining Characteristics
First detected ……………….  only one diagnosed episode
Paroxysmal…………………..recurrent episodes that self-terminate in less than 7 days
Persistent……………………….recurrent episodes that last more than 7 days
Permanent……………………..an ongoing long-term episode

All atrial fibrillation patients are initially in the category called first detected AF. These patients may or may not have had previous undetected episodes. If a first detected episode self-terminates in less than 7 days and then another episode begins later on, the case has moved into the category of paroxysmal AF. Although patients in this category have episodes lasting up to 7 days, in most cases of paroxysmal AF the episodes will self-terminate in less than 24 hours. If instead the episode lasts for more than 7 days, it is unlikely to self-terminate and it is called persistent AF. In this case, the episode may be terminated by cardioversion. If cardioversion is unsuccessful or it is not attempted, and the episode is ongoing for a long time (e.g. a year or more), the patient’s AF is called permanent.

Episodes that last less than 30 seconds are not considered in this classification system. Also, this system does not apply to cases where the AF is a secondary condition that occurs in the setting of a primary condition that may be the cause of the AF.

Using this classification system, it’s not always clear what an AF case should be called. For example, a case may fit into the paroxysmal AF category some of the time, while other times it may have the characteristics of persistent AF. One may be able to decide which category is more appropriate by determining which one occurs most often in the case under consideration.

In addition to the above four AF categories, which are mainly defined by episode timing and termination, the ACC/AHA/ESC guidelines describe additional AF categories in terms of other characteristics of the patient.

#Lone atrial fibrillation (LAF) – absence of clinical or echocardiographic findings of other cardiovascular disease (including hypertension), related pulmonary disease, or cardiac abnormalities such as enlargement of the left atrium, and age under 60 years

#Nonvalvular AF – absence of rheumatic mitral valve disease, a prosthetic heart valve, or mitral valve repair

#Secondary AF – occurs in the setting of a primary condition which may be the cause of the AF, such as acute myocardial infarction, cardiac surgery, pericarditis, myocarditis, hyperthyroidism, pulmonary embolism, pneumonia, or other acute pulmonary disease

Although atrial fibrillation itself usually isn’t life-threatening, it is a medical emergency. It can lead to complications. Treatments for atrial fibrillation may include medications and other interventions to try to alter the heart’s electrical system.

Symptoms:
A heart in atrial fibrillation doesn’t beat efficiently. It may not be able to pump enough blood out to your body with each heartbeat.

Some people with atrial fibrillation have no symptoms and are unaware of their condition until it’s discovered during a physical examination. Those who do have atrial fibrillation symptoms may experience:

#Palpitations, which are sensations of a racing, uncomfortable, irregular heartbeat or a flopping in your chest
#Decreased blood pressure
#Weakness
#Lightheadedness
#Confusion
#Shortness of breath
#Chest pain

Atrial fibrillation may be:

#Occasional. In this case it’s called paroxysmal (par-ok-SIZ-mul) atrial fibrillation. You may have symptoms that come and go, lasting for a few minutes to hours and then stopping on their own.
#Chronic. With chronic atrial fibrillation, symptoms may last until they’re treated.

Time to see a doctor:-
If you have any symptoms of atrial fibrillation, make an appointment with your doctor. Your doctor should be able to tell you if your symptoms are caused by atrial fibrillation or another heart arrhythmia.

If you have chest pain, seek emergency medical assistance immediately. Chest pain could signal that you’re having a heart attack.

Causes:
To pump blood, your heart muscles must contract and relax in a coordinated rhythm. Contraction and relaxation are controlled by electrical signals that travel through your heart muscle.

Your heart consists of four chambers — two upper chambers (atria) and two lower chambers (ventricles). Within the upper right chamber of your heart (right atrium) is a group of cells called the sinus node. This is your heart’s natural pacemaker. The sinus node produces the impulse that starts each heartbeat.

Normally, the impulse travels first through the atria and then through a connecting pathway between the upper and lower chambers of your heart called the atrioventricular (AV) node. As the signal passes through the atria, they contract, pumping blood from your atria into the ventricles below. As the signal passes through the AV node to the ventricles, the ventricles contract, pumping blood out to your body.

.Sinus rhythm.

..Atrial fibrillation

In atrial fibrillation, the upper chambers of your heart (atria) experience chaotic electrical signals. As a result, they quiver. The AV node — the electrical connection between the atria and the ventricles — is overloaded with impulses trying to get through to the ventricles. The ventricles also beat rapidly, but not as rapidly as the atria. The reason is that the AV node is like a highway on-ramp — only so many cars can get on at one time.

The result is a fast and irregular heart rhythm. The heart rate in atrial fibrillation may range from 100 to 175 beats a minute. The normal range for a heart rate is 60 to 100 beats a minute.

Possible causes of atrial fibrillation :-

Abnormalities or damages to the heart’s structure are the most common cause of atrial fibrillation. Possible causes of atrial fibrillation include:

#High blood pressure
#Heart attacks
#Abnormal heart valves
#Congenital heart defects
#An overactive thyroid or other metabolic imbalance
#Exposure to stimulants such as medications, caffeine or tobacco, or to alcohol
#Sick sinus syndrome — improper functioning of the heart’s natural pacemaker
#Emphysema or other lung diseases
#Previous heart surgery
#Viral infections
#Stress due to pneumonia, surgery or other illnesses
#Sleep apnea
However, some people who have atrial fibrillation don’t have any heart defects or damage, a condition called lone atrial fibrillation. In lone atrial fibrillation, the cause is often unclear, and serious complications are rare.

Atrial flutter :
Atrial flutter is similar to atrial fibrillation, but slower. If you have atrial flutter, the abnormal heart rhythm in your atria is more organized and less chaotic than the abnormal patterns common with atrial fibrillation. Sometimes you may have atrial flutter that develops into atrial fibrillation and vice versa. The symptoms, causes and risk factors of atrial flutter are similar to those of atrial fibrillation. For example, strokes are a common concern in someone with atrial flutter. As with atrial fibrillation, atrial flutter is usually not life-threatening when it’s properly treated.

Risk Factors:-

Risk factors for atrial fibrillation include:

#Age. The older you are, the greater your risk of developing atrial fibrillation.
#Heart disease. Anyone with heart disease, including valve problems, history of heart attack and heart surgery, has an increased risk of atrial fibrillation.
#High blood pressure. Having high blood pressure, especially if it’s not well controlled with lifestyle changes or medications, can increase your risk of atrial fibrillation.
#Other chronic conditions. People with thyroid problems, sleep apnea and other medical problems have an increased risk of atrial fibrillation.
#Drinking alcohol. For some people, drinking alcohol can trigger an episode of atrial fibrillation. Binge drinking — having five drinks in two hours for men, or four drinks for women — may put you at higher risk.
#Family history. An increased risk of atrial fibrillation runs in some families.

Complications:-

Clots and stroke :
One of the most common complications with atrial fibrillation is the formation of blood clots in the heart. As the blood in the upper chambers of the heart (atria) of a patient with atrial fibrillation does not flow out in a normal manner and is very turbulent, there is a greater likelihood of blood clots forming. The clots may then find their way into the lower chambers of the heart (ventricles) and eventually end up in the lungs or in the general circulation. Clots in the general circulation may eventually block arteries in the brain, causing a stroke.

A patient with atrial fibrillation is twice as likely to develop a stroke compared to other people. 5% of patients with atrial fibrillation get a stroke each year. The risk is even greater the older the patient is. The following factors raise the risk of stroke even more for patients with atrial fibrillation:

#Hypertension (high blood pressure)
#Diabetes
#Heart failure
#A history of blood clots (embolism)

Strokes may be severe and can cause paralysis of part of the body, speech problems, and even death.

Heart failure:
If the atrial fibrillation is not controlled the heart is likely to get weaker. This may lead to heart failure. Heart failure is when the heart does not pump blood around the body efficiently or properly. The patient’s left side, right side, or even both sides of the body can be affected.

Alzheimer’s disease:
There is a strong relationship between atrial fibrillation and the development of Alzheimer’s disease, according to researchers at Researchers at Intermountain Medical Center in Salt Lake City.

Diagnosis:-
The evaluation of atrial fibrillation involves diagnosis, determination of the etiology of the arrhythmia, and classification of the arrhythmia. A minimal evaluation should be performed in all individuals with AF. This includes a history and physical examination, ECG, transthoracic echocardiogram, and routine bloodwork. Certain individuals may benefit from an extended evaluation which may include an evaluation of the heart rate response to exercise, exercise stress testing, a chest x-ray, trans-esophageal echocardiography, and other studies.

Screening
Screening for atrial fibrillation is not generally performed, although a study of routine pulse checks or ECGs during routine office visits found that the annual rate of detection of AF in elderly patients improved from 1.04% to 1.63%; selection of patients for prophylactic anticoagulation would improve stroke risk in that age category.[9]

Routine primary care visit
This estimated sensitivity of the routine primary care visit is 64%. This low result probably reflects the pulse not being checked routinely or carefully.

Minimal evaluation
The minimal evaluation of atrial fibrillation should generally be performed in all individuals with AF. The goal of this evaluation is to determine the general treatment regimen for the individual. If results of the general evaluation warrant it, further studies may be then performed.

History and physical examination
The history of the individual’s atrial fibrillation episodes is probably the most important part of the evaluation. Distinctions should be made between those who are entirely asymptomatic when they are in AF (in which case the AF is found as an incidental finding on an ECG or physical examination) and those who have gross and obvious symptoms due to AF and can pinpoint whenever they go into AF or revert to sinus rhythm.

Routine bloodwork
While many cases of AF have no definite cause, it may be the result of various other problems (see below). Hence, renal function and electrolytes are routinely determined, as well as thyroid-stimulating hormone (commonly suppressed in hyperthyroidism and of relevance if amiodarone is administered for treatment) and a blood count.

In acute-onset AF associated with chest pain, cardiac troponins or other markers of damage to the heart muscle may be ordered. Coagulation studies (INR/aPTT) are usually performed, as anticoagulant medication may be commenced

Electrocardiogram
Atrial fibrillation is diagnosed on an electrocardiogram (ECG), an investigation performed routinely whenever an irregular heart beat is suspected. Characteristic findings are the absence of P waves, with unorganized electrical activity in their place, and irregular R-R intervals due to irregular conduction of impulses to the ventricles.

When ECGs are used for screening, the SAFE trial found that electronic software, primary care physicians and the combination of the two had the following sensitivities and specificities:

#Interpreted by software: sensitivity = 83%, specificity = 99%
#Interpreted by a primary care physician: sensitivity = 80%, specificity = 92%
#Interpreted by a primary care physician with software: sensitivity = 92%, specificity = 91%

If paroxysmal AF is suspected but an ECG during an office visit only shows a regular rhythm, AF episodes may be detected and documented with the use of ambulatory Holter monitoring (e.g. for a day). If the episodes are too infrequent to be detected by Holter monitoring with reasonable probability, then the patient can be monitored for longer periods (e.g. a month) with an ambulatory event monitor.

Echocardiography.
A non-invasive transthoracic echocardiogram (TTE) is generally performed in newly diagnosed AF, as well as if there is a major change in the patient’s clinical state. This ultrasound-based scan of the heart may help identify valvular heart disease (which may greatly increase the risk of stroke), left and right atrial size (which indicates likelihood that AF may become permanent), left ventricular size and function, peak right ventricular pressure (pulmonary hypertension), presence of left ventricular hypertrophy and pericardial disease.

Significant enlargement of both the left and right atria is associated with long-standing atrial fibrillation and, if noted at the initial presentation of atrial fibrillation, suggests that the atrial fibrillation is likely to be of a longer duration than the individual’s symptoms.

Extended evaluation
An extended evaluation is generally not necessary in most individuals with atrial fibrillation, and is only performed if abnormalities are noted in the limited evaluation, if a reversible cause of the atrial fibrillation is suggested, or if further evaluation may change the treatment course.

Chest X-ray
A chest X-ray is generally only performed if a pulmonary cause of atrial fibrillation is suggested, or if other cardiac conditions are suspected (particularly congestive heart failure.) This may reveal an underlying problem in the lungs or the blood vessels in the chest.  In particular, if an underlying pneumonia is suggested, then treatment of the pneumonia may cause the atrial fibrillation to terminate on its own.

Transesophageal echocardiogram
A normal echocardiography (transthoracic or TTE) has a low sensitivity for identifying thrombi (blood clots) in the heart. If this is suspected – e.g. when planning urgent electrical cardioversion – a transesophageal echocardiogram (TEE) is preferred.

The TEE has much better visualization of the left atrial appendage than transthoracic echocardiography. This structure, located in the left atrium, is the place where thrombus is formed in more than 90% of cases in non-valvular (or non-rheumatic) atrial fibrillation or flutter. TEE has a high sensitivity for locating thrombus in this area   and can also detect sluggish bloodflow in this area that is suggestive of thrombus formation.

If no thrombus is seen on TEE, the incidence of stroke, (immediately after cardioversion is performed), is very low.

Ambulatory holter monitoring
A Holter monitor is a wearable ambulatory heart monitor that continuously monitors the heart rate and heart rhythm for a short duration, typically 24 hours. In individuals with symptoms of significant shortness of breath with exertion or palpitations on a regular basis, a holter monitor may be of benefit to determine if rapid heart rates (or unusually slow heart rates) during atrial fibrillation are the cause of the symptoms.

Exercise stress testing
Some individuals with atrial fibrillation do well with normal activity but develop shortness of breath with exertion. It may be unclear if the shortness of breath is due to a blunted heart rate response to exertion due to excessive AV node blocking agents, a very rapid heart rate during exertion, or due to other underlying conditions such as chronic lung disease or coronary ischemia. An exercise stress test will evaluate the individual’s heart rate response to exertion and determine if the AV node blocking agents are contributing to the symptoms.

Treatments:-
In some people, a specific event or an underlying condition, such as a thyroid disorder, may trigger atrial fibrillation. If the condition that triggered your atrial fibrillation can be treated, you might not have any more heart rhythm problems — or at least not for quite some time. If your symptoms are bothersome or if this is your first episode of atrial fibrillation, your doctor may attempt to reset the rhythm

The treatment option best for you will depend on how long you’ve had atrial fibrillation, how bothersome your symptoms are and the underlying cause of your atrial fibrillation. Generally, the goals of treating atrial fibrillation are to:

#Reset the rhythm or control the rate
#Prevent blood clots
The strategy you and your doctor choose depends on many factors, including whether you have other problems with your heart and if you’re able to take medications that can control your heart rhythm. In some cases, you may need a more invasive treatment, such as surgery or medical procedures using catheters.

Resetting your heart’s rhythm
Ideally, to treat atrial fibrillation, the heart rate and rhythm are reset to normal. To correct your condition, doctors may be able to reset your heart to its regular rhythm (sinus rhythm) using a procedure called cardioversion, depending on the underlying cause of atrial fibrillation and how long you’ve had it.

Cardioversion can be done in two ways:

#Cardioversion with drugs. This form of cardioversion uses medications called anti-arrhythmics to help restore normal sinus rhythm. Depending on your heart condition, your doctor may recommend trying intravenous or oral medications to return your heart to normal rhythm. This is often done in the hospital with continuous monitoring of your heart rate. If your heart rhythm returns to normal, your doctor often will prescribe the same anti-arrhythmic or a similar one to try to prevent more spells of atrial fibrillation.
#Electrical cardioversion. In this brief procedure, an electrical shock is delivered to your heart through paddles or patches placed on your chest. The shock stops your heart’s electrical activity momentarily. When your heart begins again, the hope is that it resumes its normal rhythm. The procedure is performed during anesthesia.
Before cardioversion, you may be given a blood-thinning medication, such as warfarin (Coumadin), for several weeks to reduce the risk of blood clots and stroke. Unless the episode of atrial fibrillation lasted less than 24 hours, you’ll need to take warfarin for at least four to six weeks after cardioversion to prevent a blood clot from forming even after your heart is back in normal rhythm. Warfarin is a powerful medication that can have dangerous side effects if not taken exactly as directed by your doctor. If you have any concerns about taking warfarin, talk to your doctor.

Or, instead of taking warfarin, you may have a test called transesophageal echocardiography — which can tell your doctor if you have any heart blood clots — just before cardioversion. In transesophageal echocardiography, a tube is passed down your esophagus and detailed ultrasound images are made of your heart. You’ll be sedated during the test.

Maintaining a normal heart rhythm
After electrical cardioversion, anti-arrhythmic medications often are prescribed to help prevent future episodes of atrial fibrillation. Commonly used medications include:

#Amiodarone (Cordarone, Pacerone)
#Propafenone (Rythmol)
#Sotalol (Betapace)
#Dofetilide (Tikosyn)
Although these drugs can help maintain a normal heart rhythm in many people, they can cause side effects, including:

#Nausea
#Dizziness
#Fatigue
Rarely, they may cause ventricular arrhythmias — life-threatening rhythm disturbances originating in the heart’s lower chambers. These medications may be needed indefinitely. Even with medications, the chance of another episode of atrial fibrillation is high.

Heart rate control
Sometimes atrial fibrillation can’t be converted to a normal heart rhythm. Then the goal is to slow the heart rate to between 60 and 100 beats a minute (rate control). Heart rate control can be achieved two ways:

#Medications. Traditionally, doctors have prescribed the medication digoxin (Lanoxin). It can control heart rate at rest, but not as well during activity. Most people require additional or alternative medications, such as calcium channel blockers or beta blockers.
#Atrioventricular (AV) node ablation. If medications don’t work, or you have side effects, AV node ablation may be another option. The procedure involves applying radio frequency energy to the pathway connecting the upper and lower chambers of your heart (AV node) through a long, thin tube (catheter) to destroy this small area of tissue.

The procedure prevents the atria from sending electrical impulses to the ventricles. The atria continue to fibrillate, though, and anticoagulant medication is still required. A pacemaker is then implanted to establish a normal rhythm. After AV node ablation, you’ll need to continue to take blood-thinning medications to reduce the risk of stroke, because your heart rhythm is still atrial fibrillation.

Other surgical and catheter procedures
Sometimes medications or cardioversion to control atrial fibrillation doesn’t work. In those cases, your doctor may recommend a procedure to destroy the area of heart tissue that’s causing the erratic electrical signals and restore your heart to a normal rhythm. These options can include:

#Radiofrequency catheter ablation. In many people who have atrial fibrillation and an otherwise normal heart, atrial fibrillation is caused by rapidly discharging triggers, or “hot spots.” These hot spots are like abnormal pacemaker cells that fire so rapidly that the upper chambers of your heart quiver instead of beating efficiently.

Radiofrequency energy directed to these hot spots through a catheter inserted in an artery near your collarbone or leg may be used to destroy these hot spots, scarring the tissue so the erratic electrical signals are normalized. This corrects the arrhythmia without the need for medications or implantable devices. In some cases, other types of catheters that can freeze the heart tissue (cryotherapy) are used.

#Surgical maze procedure. The maze procedure is often done during an open-heart surgery. Using a scalpel, doctors create several precise incisions in the upper chambers of your heart to create a pattern of scar tissue. Because scar tissue doesn’t carry electricity, it interferes with stray electrical impulses that cause atrial fibrillation. Radiofrequency or cryotherapy can also be used to create the scars, and there are several variations of the surgical maze technique. The procedure has a high success rate, but because it usually requires open-heart surgery, it’s generally reserved for people who don’t respond to other treatments or when it can be done during other necessary heart surgery, such as coronary artery bypass surgery or heart valve repair. Some people need a pacemaker implanted after the procedure.

Preventing blood clots
Most people who have atrial fibrillation or who are undergoing certain treatments for atrial fibrillation are at especially high risk of blood clots that can lead to stroke. The risk is even higher if other heart disease is present along with atrial fibrillation. Your doctor may prescribe blood-thinning medications (anticoagulants) such as warfarin (Coumadin) in addition to medications designed to treat your irregular heartbeat. Many people have spells of atrial fibrillation and don’t even know it — so you may need lifelong anticoagulants even after your rhythm has been restored to normal. If you’re prescribed warfarin, carefully follow your doctor’s instructions on taking it. Warfarin is a powerful medication that can have dangerous side effects.

Change of Lifestyle :

You may need to make lifestyle changes that improve the overall health of your heart, especially to prevent or treat conditions such as high blood pressure. Your doctor may suggest that you:

#Eat heart-healthy foods and avoid Junk or Fast food
#Reduce your salt intake, which can help lower blood pressure
#Increase your physical activity
#Quit smoking
#Pratice regular Exercise Or walk for about 45 minutes daily

Avoid drinking more than one drink of alcohol for women or more than two drinks for men a day.

Prevention:-
There are some things you can do to try to prevent recurrent spells of atrial fibrillation. You may need to reduce or eliminate caffeinated and alcoholic beverages from your diet, because they can sometimes trigger an episode of atrial fibrillation. It’s also important to be careful when taking over-the-counter (OTC) medications. Some, such as cold medicines containing pseudoephedrine, contain stimulants that can trigger atrial fibrillation. Also, some OTC medications can have dangerous interactions with anti-arrhythmic medications.

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://en.wikipedia.org/wiki/Atrial_fibrillation
http://www.mayoclinic.com/health/atrial-fibrillation/DS00291
http://www.medicalnewstoday.com/info/atrial-fibrillation/

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Be VERY Careful When Replacing Missing Teeth

 

By Dr. Lina Garcia

A dental implant is one option for replacing missing or badly diseased teeth. It is composed of an artificial root that looks like a post or screw and is covered with a dental crown.
……………....CLICK & SEE
Treatment involves the surgical placement of the implant into the jawbone, where it is allowed to fuse to the bone in a process called “osseointegration.”

Once healed, the implant acts as an anchor for an artificial replacement tooth, or crown. The crown is made to blend in with your other teeth and is permanently attached to the implant.

A typical dental implant is made of pure titanium and/or a titanium alloy.

In fact, titanium alloys are widely used in both medicine and dentistry, for dental implants, pacemakers, stents, orthodontal brackets, and orthopedic implants (e.g., hip, shoulder, knee, or elbow). Not only is titanium strong, but many consider it biocompatible: it forms an oxide layer when exposed to air, and this purportedly results in reduced corrosion and superior osseointegration.

So why should you reject the standard titanium metal implant?

Titanium is NOT Biologically Inert

Titanium implants release metal ions into your mouth 24 hours a day, and this chronic exposure may trigger inflammation, allergies, and autoimmune disease in susceptible individuals. They are a precursor to disease.

Cases of intolerance to metal implants have been reported over the years, and the removal of this incompatible dental material has resulted in reduced metal sensitivity and long-term health improvement in the majority of patients.

Titanium has the potential to induce hypersensitivity as well as other immunological dysfunctions.

One study investigated 56 patients who developed severe health problems after receiving titanium-based dental implants. These medical problems included muscle, joint, and nerve pain; chronic fatigue syndrome; neurological problems; depression; and skin inflammation.

Removal of the implants resulted in a dramatic improvement in the patients’ symptoms, as well as a decrease in many patients’ sensitivity to titanium.

For example, a 54-year-old man with a titanium dental implant and four titanium screws in his vertebra was so sick that he could not work. He suffered from chronic fatigue syndrome, cognitive impairment, Parkinson-like trembling, and severe depression. Six months after the removal of the implants and screws, he was able to return to work.

In another case, a 14-year-old girl developed inflammatory lesions on her face six months after being fitted with titanium orthodontal brackets.

She was also mentally and physically exhausted, and her reactivity to titanium skyrocketed. Within nine months of replacing the brackets with a metal-free material, her facial lesions had almost completely healed, she was healthy and active, and her sensitivity to titanium returned to a normal level.

Titanium Implants Can Cause Cancer

Another complication of the use of implanted titanium is its potential to induce the abnormal proliferation of cells (neoplasia), which can lead to the development of malignant tumors and cancer. Through rare, it is a well-known complication of orthopedic surgery that involves the implantation of metallic hardware.

Furthermore, researchers recently uncovered the first reported case of a sarcoma arising in association with a dental implant.

As described in the August 2008 issue of JADA (The Journal of the American Dental Association), a 38-year-old woman developed bone cancer eleven months after receiving a titanium dental implant. Luckily, she was successfully treated with chemotherapy, but the authors recommended further research into the tumor-causing potential of dental implants in light of their increasing popularity and their ability to last for longer periods of time.

Why You Want to Avoid ANY Kind of Metal in Your Mouth

Finally, the presence of any metal in your mouth sets the stage for “galvanic toxicity,” because your mouth essentially becomes a charged battery when dissimilar metals sit in a bed of saliva.
All that is needed to make a battery is two or more different metals and a liquid medium that can conduct electricity (i.e., an electrolyte). Metal implants, fillings, crowns, partials, and orthodontics provide the dissimilar metals, and the saliva in your mouth serves as the electrolyte.

An electric current called a galvanic current is then generated by the transport of the metal ions from the metal-based dental restorations into the saliva. This phenomenon is called “oral galvanism,” and it literally means that your mouth is acting like a small car battery or a miniature electrical generator. The currents can actually be measured using an ammeter!

Oral galvanism creates two major concerns.

First, the electric currents increase the rate of corrosion (or dissolution) of metal-based dental restorations. Even precious metal alloys continuously release metal ions into your mouth due to corrosion, a process that gnaws away bits of metal from the metal’s surface.

These ions react with other components of your body, leading to sensitivity, inflammation, and, ultimately, autoimmune disease. Increasing the corrosion rate, therefore, increases the chance of developing immunologic or toxic reactions to the metals.

Second, some individuals are very susceptible to these internal electrical currents. Dissimilar metals in your mouth can cause unexplained pain, nerve shocks, ulcerations, and inflammation, and many people also experience a constant metallic or salty taste, or a burning sensation in their mouth.

Moreover, there is the concern that oral galvanism directs electrical currents into brain tissue and can disrupt the natural electrical current in your brain.

New Alternatives to Titanium Implants

In recent years, high-strength ceramic implants have become attractive alternatives to titanium implants, and some current research has focused on the viability of materials such as zirconia (the dioxide of zirconium, a metal close to titanium on the periodic table).
………………
Metal-free zirconia implants have been used in Europe and South America for years, but they have only recently become available in the U.S.

Zirconia implants are highly biocompatible to the human body and exhibit minimum ion release compared to metallic implants.

Studies have shown that the osseointegration of zirconia and titanium implants are very similar, and that zirconia implants have a comparable survival rate, thereby making them an excellent alternative to metal implants.

Moreover, zirconia ceramics have been successfully used in orthopedic surgery to manufacture ball heads for total hip replacements.

Therefore, given that titanium dental implants can induce metal sensitivity, inflammation, autoimmunity, and malignant tumors, while zirconia implants are metal-free but just as durable, why invite chronic metal exposure?

Your body would surely benefit from choosing the biocompatible, ceramic dental implant over the standard, titanium metal implant.

Dr. Lina Garcia, a committed holistic dentist for 25 years, has dedicated her practice to using dental materials that will support your health and not disease. In her practice, she offers only metal-free restorative materials, including zirconia implants.

Source:Mercola.com

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People with Migraine Prone to Clotting

People with migraines are more likely to develop blood clots in their veins, a study has suggested….CLICK & SEE

The research, published in the latest issue of Neurology, the medical journal of the American Academy of Neurology, found that those suffering from migraines may be more likely to develop blood clots in their veins.

In the condition, called venous thrombosis or thromboembolism, blood clots form in a vein, which can limit blood flow and cause swelling and pain. Those clots can then dislodge from the vein and travel to the heart and the lungs, which can be fatal.

The study examined 574 people in Italy age 55 and up to determine whether they had a history of migraine or migraine at the time of the evaluation. The doctors also reviewed their medical records for cases of venous thrombosis.

The Science Daily online reported that of the participants, 111 people had migraine. A total of 21 people with migraine also had one or more instances of venous thrombosis. In comparison, 35 people without migraine had the condition.

Though researchers were unable to pinpoint the reason for the link between migraine and venous thrombosis, a theory is that the blood of people with migraine may be more prone to clotting, the report said.

It was also found that people with migraine are not more likely to have hardening or narrowing of the arteries, which is contrary to a current theory.

“The thinking has been that because people with migraine are more likely to have strokes and other cardiovascular problems, that they would also have more severe and early atherosclerosis,” said study author Stefan Kiechl, of Innsbruck Medical University in Austria. He said the study provides solid evidence to refute it.

Sources: The Times Of India

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