|Prostatitis - Eczema|
|Written by Ruai Pharmaceuticals|
|Wednesday, 17 August 2011 08:03|
Table of contents
What is the prostate gland?
The prostate is a small organ located at the base of the bladder and wrapped around the urethra, the tube that empties the bladder through the penis. It sits in front of the rectum, and the back portion of the organ can be felt during rectal examination by a health care practitioner.
The prostate's purpose is to help with the male reproductive system. It makes up to 70% of the fluid that is ejaculated during intercourse, mixing its secretions with the sperm that are made in the testicles. The prostate also contracts at the time of ejaculation to prevent retrograde (or backward) flow of semen into the bladder.
Because of its location, the symptoms of any prostate problem tend to be associated with the bladder and can include urgency to urinate, frequency of urination, burning with urination (dysuria), poor urine flow, or inability to begin a urine stream.
What is prostatitis?
Prostatitis is the general term used to describe prostate inflammation (-itis). Because the term is so general, it does not adequately describe the range of abnormalities that can be associated with prostate inflammation. Therefore, four types of prostatitis are recognized.
What are the types and symptoms of prostatitis?
There are four types of prostatitis:
Acute bacterial prostatitis causes and symptoms
Acute bacterial prostatitis is an infection of the prostate that is often caused by some of the same bacteria that cause bladder infections. These include E. coli, Klebsiella, and Proteus. While it may be acquired as a sexually transmitted disease, the infection can also spread to the prostate through the blood stream, directly from an adjacent organ, or as a complication of prostate biopsy.
Patients with acute bacterial prostatitis present with signs of an infection and may have:
Commonly there is urgency and frequency of urination and dysuria (painful or difficult urination).
Chronic bacterial prostatitis causes and symptoms
Chronic bacterial prostatitis is an uncommon illness in which there is an ongoing bacterial infection in the prostate. Chronic bacterial prostatitis generally causes no symptoms, however, on occasion; the low grade infection may flare and be associated with a bladder infection.
Chronic prostatitis without infection causes and symptoms
Chronic prostatitis without infection, also known as chronic pelvic pain syndrome, is a condition where there is recurrent pelvic, testicle, or rectal pain without evidence of bladder infection. There may be difficulties with painful urination or ejaculation, and erectile dysfunction. The cause of chronic prostatitis without infection is not clearly understood.
Asymptomatic inflammatory prostatitis causes and symptoms
Asymptomatic inflammatory prostatitis is exactly as its name describes. There are no symptoms. The cause of asymptomatic inflammatory prostatitis is not clearly understood.
How is prostatitis diagnosed?
The diagnosis of prostatitis relies on a careful history and physical examination by the health care practitioner.
The most important laboratory test is a urinalysis to help differentiate the types of prostatitis. The need for other blood tests or imaging studies like ultrasound, X-ray, and computerized tomography (CT) will depend upon the clinical situation and presentation.
Acute bacterial prostatitis diagnosis
After taking a history, the health care practitioner will likely have a directed physical examination concentrating on the scrotum, looking for inflammation of the testicle(s) or epididymis, and the flank and mid-back, where the kidney is located. If a rectal examination is performed, the prostate may be swollen and boggy, consistent with acute inflammation.
Laboratory testing may include urinalysis, looking for white blood cells and bacteria, signifying infection. The urine may also be cultured to identify the bacteria that are responsible for the infection, but results will take up to seven days to return. The results will help confirm that the antibiotic chosen is correct and may help choose an alternate antibiotic should the illness progress.
Chronic bacterial prostatitis diagnosis
The diagnosis is made by finding an abnormal urinalysis. Sometimes, a urinalysis is collected after prostate examination. This may allow some prostatic fluid to be expressed into the urine and cultured.
A blood test called PSA (prostate surface antigen) may be elevated in this type of prostatitis. While PSA is used as a prostate cancer screening tool, it can also be elevated whenever the prostate is inflamed.
Chronic prostatitis without infection diagnosis
To make the diagnosis of chronic prostatitis without infection, symptoms should be present for at least three months. The cause of chronic prostatitis without infection (chronic pelvic pain syndrome) is not known.
This is a frustrating condition for the patient and the health care practitioner since there is controversy as to the aggressiveness of testing, and exactly what tests should be done. Often, this is a diagnosis of exclusion, meaning that blood tests, urine tests, x-rays and ultrasounds tend to be normal, yet the patient continues to suffer.
Asymptomatic inflammatory prostatitis diagnosis
There are no symptoms with this type of prostatitis, however, when routine lab tests are performed, white blood cells (a sign of inflammation) are found in the urine, but there are no associated bacteria or infection.
What is the treatment for prostatitis?
Acute bacterial prostatitis treatment
Treatment for acute bacterial prostatitis is a prescription for antibiotics by mouth, usually ciprofloxacin (Cipro) or tetracycline (Achromycin). Home care includes drinking plenty of fluids, medications for pain control, and rest.
Learn more about: Cipro
If the patient is acutely ill or has a compromised immune system (for example, is taking chemotherapy or other immune suppression drugs or has HIV/AIDS), hospitalization for intravenous antibiotics and care may be required.
Chronic bacterial prostatitis treatment
Chronic bacterial prostatitis treatment is with long-term antibiotics, up to eight weeks, with ciprofloxacin (Cipro, Cipro XR), sulfa drugs [for example, sulfamethoxazole and trimethoprim, (Bactrim)], or erythromycin. Even with appropriate therapy, this type of prostatitis can recur. It is uncertain as to why, but it may be due to a poorly emptying bladder. A small amount of stagnant urine allows the potential for recurrent infection to occur. This situation can be caused by benign prostatic hypertrophy (BPH), bladder stones, or prostate stones.
Learn more about: Cipro XR | Bactrim
Chronic prostatitis without infection treatment
Chronic prostatitis without infection treatment addresses chronic pain control and may include physical therapy and relaxation techniques as well as tricyclic antidepressant medications.
Other medication possibilities include alpha-adrenergic blockers. Tamsulosin (Flomax) and terazosin (Hytrin) are drugs that block the non-heart adrenaline receptors and are used in treating BPH and bladder outlet obstruction. Allowing better bladder emptying may help minimize symptoms.
Learn more about: Flomax | Hytrin
Asymptomatic inflammatory prostatitis treatment
Treatment is not required for this type of prostatitis.
In patients undergoing infertility assessment, this inflammation may be treated with a course of either a nonsteroidal anti-inflammatory medication (ibuprofen, Motrin, Advil) or antibiotics.
What is the prognosis for prostatitis?
Heart Attack Pathology
What is a Heart Attack?
A heart attack is a layperson's term for a sudden blockage of a coronary artery. This blockage, which doctors call a coronary artery occlusion, may be fatal, but most patients survive it. Death can occur when the occlusion leads to an abnormal heartbeat (severe arrhythmia) or death of heart muscle (extensive myocardial infarction). In both of these situations, the heart can no longer pump blood adequately to supply the brain and other organs of the body. Almost all heart attacks occur in people who have coronary artery disease (coronary atherosclerosis). So, this photo essay will review the structure (anatomy) of the normal coronary artery, the structural abnormalities (pathology) of the coronary artery in atherosclerosis, and the effect of these abnormalities on the heart.
What are the structures and functions of a normal coronary artery?
The coronary arteries carry blood to the heart to supply oxygen and necessary nutrients. As seen in Figure 1, the wall of a coronary artery has 3 distinct layers: the inner (intima), middle (media), and outer (adventitia) layers. The wall of the artery surrounds the lumen of the artery, which is the channel through which blood flows.
Figure 1: Normal Coronary Artery
Cross-sectional Microscopic View
In Figure 1, smooth muscle is red, and connective (supporting) tissue is black (elastic) or blue (collagen).
The intima is best seen in the close-up view in Figure 1. It is composed of a layer of so-called endothelial cells that covers the artery's inner (lumenal) surface, connective (supporting) tissue (collagen and elastin), and a layer of compact elastic tissue called the internal elastic lamina (IEL). In the past, the intima was thought to be simply a passive layer whose major purpose was to serve as a barrier. Now, however, we know that the endothelial cells actually keep track of the pressure, flow, and "health" of the artery. Moreover, endothelial cells secrete chemicals that can adjust the function of the artery (e.g., vasodilator chemicals to widen and vasoconstrictors to narrow it) and growth of the artery wall (e.g., growth factors).
The media (M) is a layer made up primarily of smooth muscle cells (SMCs). The muscle can contract and relax to control the blood pressure and flow in the artery. Elastic tissue and collagen in the media, along with elastic tissue in the IEL, increase the elasticity and strength of the wall of the artery, as the artery contracts and relaxes. The adventitia is a layer of connective tissue and cells (e.g., SMCs) that produce this connective tissue. The adventitia contains potent factors, including one called tissue thromboplastin, that promote blood clotting. The clots are useful when the artery becomes injured because they can limit excessive bleeding from the injured artery.
What happens to the coronary artery in atherosclerosis?
In coronary artery disease (coronary atherosclerosis), injury to the intima of the artery leads to the formation of plaques, which are regions of thickening on the inner lining of the artery. How then do the plaques form? In response to the injury, the smooth muscle cells (SMCs) from the media and perhaps from the adventitia move (migrate) into the intima. In the intima, these SMCs reproduce themselves (divide) and make (synthesize) connective tissue. These processes of migration, division, and synthesis, which collectively are referred to as intimal proliferation (buildup), cause thickening of the intima. When cholesterol, other fats, and inflammatory cells, such as white blood cells, enter the proliferating, thickened intima, the result is an atherosclerotic plaque. Then, as these plaques grow, they accumulate scar (fibrous) tissue and abundant calcium. (Calcium is the hard material in our teeth and bones.) Hence, the plaques are often hard, which is why atherosclerosis is sometimes referred to as "hardening of the arteries."
Who gets coronary artery plaques and what happens to the plaques?
Most adults in industrialized nations have some plaques (atherosclerosis) on the inner (lumenal) surface of their coronary arteries. Autopsy studies of young soldiers who died in World War II, the KOrean War, and the Vietnam War showed that even young adults in their 20s usually have coronary arteries that exhibit localized (focal) thickening of the intima. This thickening is the beginning of intimal proliferation and plaque formation. The distribution, severity (amount of plaque), and rate of growth of the plaques in the coronary arteries vary greatly from person to person. Figure 2 shows a coronary artery with an uneven (asymmetric), stable atherosclerotic plaque. A stable plaque may grow slowly, but has an intact inner (lumenal) surface with no clot (thrombus) on this surface.
Figure 2: Coronary Artery with Stable Atherosclerotic Plaque
Cross-sectional Microscopic View
What causes a Heart Attack?
Rupture of a stable plaque in a coronary artery is the initial pathological event leading to a heart attack. When the rupture occurs, a clot suddenly forms in the lumen (channel) of the artery at the site of the rupture. Bleeding into the plaque often accompanies the rupture. The clot then blocks (occludes) the artery and thereby decreases the blood flow to the heart. This sequence of events in the coronary arteries is the basic problem in over 75% of people who suffer a heart attack. In some patients, more often women, there is just an erosion or ulceration of the plaque surface, rather than a full rupture that leads to clot formation in the coronary artery. Figure 3 shows an atherosclerotic plaque rupture and a clot in a coronary artery.
Figure 3: Rupture of Atherosclerotic Plaque in Coronary Artery
Cross-sectional Microscopic View
What happens to the heart muscle after a person survives a Heart Attack?
According to medical studies, 50% to 75% of people survive their first heart attack The others die during the heart attack because the decreased coronary blood flow causes a severe abnormal heart rhythm or extensive death of heart muscle. Figure 4 shows the heart of a patient who died 5 days after a heart attack. The photos show his myocardial infarction as it appears on the surface of the left ventricle and when the heart is sliced to view the muscle wall. About 90% of myocardial infarctions involve only the left ventricle (LV), which pumps oxygen-rich blood that comes from the lungs to the entire body. The other 10% also involve the right ventricle (RV), which pumps the blood to the lungs.
Figure 4: Myocardial Infarction Caused by Heart Attack
Views of Heart Surface and Slice Across Heart
If a person survives a heart attack, the heart muscle may return to normal or become a region of dead heart muscle (the myocardial infarction). The amount and health of the remaining heart muscle is the major determinant of the future quality of life and longevity for a patient after a heart attack. A heart attack can interrupt the normal electrical wiring of the heart, leading to abnormal heart rhythms. The heart attack can also weaken the pumping action of the heart causing shortness of breath due to heart failure. Each of these complications of a heart attack can occur at any time during the recovery period as a result of dead, dying, or scarring heart muscle.
Peripheral vascular disease (PVD) refers to diseases of the blood vessels (arteries and veins) located outside the heart and brain. While there are many causes of peripheral vascular disease, doctors commonly use the term peripheral vascular disease to refer to peripheral artery disease (peripheral arterial disease, PAD), a condition that develops when the arteries that supply blood to the internal organs, arms, and legs become completely or partially blocked as a result of atherosclerosis.
Atherosclerosis is a gradual process whereby hard cholesterol substances (plaques) are deposited in the walls of the arteries. Cholesterol plaques cause hardening of the artery walls and narrowing of the inner channel (lumen) of the artery. The atherosclerosis process begins early in life (as early as teens in some people). When atherosclerosis is mild and the arteries are not substantially narrowed, atherosclerosis causes no symptoms. Therefore many adults typically are unaware that their arteries are gradually accumulating cholesterol plaques. But when atherosclerosis becomes advanced with aging, it can cause critical narrowing of the arteries resulting in tissue ischemia (lack of blood and oxygen).
Arteries that are narrowed by advanced atherosclerosis can cause diseases in different organs. For example, advanced atherosclerosis of the coronary arteries (arteries that supply heart muscles) can lead to angina and heart attacks. Advanced atherosclerosis of the carotid and cerebral arteries (arteries that supply blood to the brain) can lead to strokes and transient ischemic attacks (TIAs). Advanced atherosclerosis in the lower extremities can lead to pain while walking or exercising (claudication), deficient wound healing, and/or leg ulcers.
Picture of Carotid Artery Disease and Plaque Buildup
Picture of Heart Attack (Myocardial Infarction) - Buildup of Cholesterol Plaque and Blood Clot
Atherosclerosis is often generalized, meaning it affects arteries throughout the body. Therefore, patients with heart attacks are also more likely to develop strokes and peripheral vascular disease, and vice versa.
There are two ways atherosclerosis causes disease; 1) atherosclerosis can limit the ability of the narrowed arteries to increase delivery of blood and oxygen to tissues during periods of increased oxygen demand such as during exertion, or 2) complete obstruction of an artery by a thrombus or embolus (thrombus and embolus are forms of blood clots; see below) resulting in tissue necrosis (death of tissue). Exertional angina and intermittent claudication are two examples of insufficient delivery of blood and oxygen to meet tissue demand; whereas strokes and heart attacks are examples of death of tissue caused by complete artery obstruction by blood clots.
There are many similarities between coronary artery diseases (atherosclerosis involving the arteries of the heart) and peripheral artery disease. For example, patients with exertional angina typically have no symptoms at rest. But during exertion the critically narrowed coronary arteries are incapable of increasing blood and oxygen delivery to meet the increased oxygen needs of the heart muscles. Lack of blood and oxygen causes chest pain (exertional angina). Exertional angina typically subsides when the patient rests. In patients with intermittent claudication, the narrowed arteries in the lower extremities (for example, a narrowed artery at the groin) cannot increase blood and oxygen delivery to the calf muscles during walking. These patients experience pain in the calf muscles that will only subside after resting.
Patients with unstable angina have critically narrowed coronary arteries that cannot deliver enough blood and oxygen to the heart muscle even at rest. These patients have chest pain at rest and are at imminent risk of developing heart attacks. Patients with severe artery occlusion in the legs can develop rest pain (usually in the feet). Rest pain represents such severe occlusion that there is insufficient blood supply to the feet even at rest. They are at risk of developing foot ulcers and gangrene.
When the arteries are narrowed as a result of atherosclerosis, blood tends to clot in the narrowed areas, forming a so-called thrombus (plural thrombi). Sometimes pieces of the thrombi break off and travel in the bloodstream until they are trapped in a narrower point in the artery beyond which they cannot pass. A thrombus or piece of thrombus that travels to another point is called an embolus (pleural emboli). Thrombi and emboli can cause sudden and complete artery blockage, leading to tissue necrosis (death of tissue).
For example, complete blockage of a coronary artery by a thrombus causes heart attack, while complete blockage of a carotid or cerebral artery causes ischemic stroke. Emboli originating form atherosclerosis in the aorta (the main artery delivering blood to the body) can obstruct small arteries in the feet, resulting in painful and blue (cyanotic) toes, foot ulcers, and even gangrene.
What are collaterals?
Sometimes, despite the presence of a severe blockage in an artery, the involved area does not become painful or ischemic due to the presence of collateral circulation, meaning that the particular area is supplied by more than one artery to an extent that blockage of a single vessel does not result in a severe degree of ischemia. Collateral circulation can develop over time to help provide oxygenated blood to an area where an artery is narrowed. Doctors believe that regular supervised exercise can stimulate the growth and development of collateral circulation and relieve symptoms of intermittent claudication.
In rare cases, the decreased circulation to the extremities characteristic of peripheral artery disease can lead to open sores that do not heal, ulcers, gangrene, or other injuries to the extremities. These areas that do not receive adequate blood flow are also more prone to develop infections, and in extreme cases, amputation may be necessary.
A number of conditions such as vasculitis (inflammation of the blood vessels, occurring either as a primary condition or associated with connective tissue diseases such as lupus) may cause damage to blood vessels throughout the body. Injuries to blood vessels (from accidents such as auto accidents or sports injuries), blood-clotting disorders, and damage to blood vessels during surgery can also lead to tissue ischemia.
Tissue ischemia can also occur in the absence of atherosclerosis or other abnormalities of arteries. One example of a condition in which the blood vessels themselves are not damaged is Raynaud's Disease, which is believed to occur due to spasms in blood vessels brought on by stress, tobacco smoking, or a cold environment.
Since atherosclerosis of the peripheral arteries (PAD) is by far the most common cause of peripheral vascular disease, the rest of this article focuses upon peripheral artery disease.
Peripheral artery disease (or peripheral arterial disease) is a common condition that affects approximately ten million adults in the U.S. About 5% of people over the age of 50 are believed to suffer from peripheral artery disease. Peripheral artery disease is slightly more common in men than in women and most often occurs in older persons (over the age of 50). The known risk factors for peripheral artery disease are those that predispose to the development of atherosclerosis. Risk factors for peripheral artery disease include:
In peripheral artery disease, the risk factors are additive, so that a person with combination of two risk factors- diabetes and smoking for example - have a more likelihood of developing more severe peripheral artery disease than a person with only one risk factor.
Approximately half of people with peripheral artery disease do not experience any symptoms. For patients with symptoms, the most common symptoms are intermittent claudication and rest pain.
Other symptoms and signs of peripheral artery disease include:
During a physical examination, your doctor may look for signs that are indicative of peripheral artery disease, including weak or absent artery pulses in the extremities, specific sounds (called bruits) that can be heard over the arteries with a stethoscope, changes in blood pressure in the limbs at rest and/or during exercise (treadmill test), and skin color and nail changes due to tissue ischemia.
In addition to the history of symptoms and the physical signs of peripheral artery disease described above, doctors can use imaging tests in the diagnosis of peripheral artery disease. These imaging tests include:
Because x-ray angiography is invasive with potential side effects (such as injury to blood vessels and contrast dye reactions), it is not used for initial diagnosis of peripheral artery disease. It is only used when a patient with severe peripheral artery disease symptoms is considered for angioplasty or surgery. A number of different imaging methods have been used in angiography examinations, including x-rays, magnetic resonance imaging (MRI), and computed tomography (CT) scans.
Treatment goals for peripheral artery disease include:
Treatments of peripheral artery disease include lifestyle measures, supervised exercises, medications, angioplasty, and surgery.
Proper exercise can condition the muscles to use oxygen effectively and can speed the development of collateral circulation. Clinical trials have demonstrated that regular supervised exercise can reduce symptoms of intermittent claudication and allow the patients to walk longer before the onset of claudication. Ideally, exercise programs should be prescribed by the doctor. Patients should be enrolled in rehabilitation programs supervised by healthcare professionals such as nurses or physical therapists. For optimal results, patients should exercise at least three times a week, each session lasting longer than 30-45 minutes. Exercise usually involves walking on a monitored treadmill until claudication develops; walking time is then gradually increased with each session. Patients are also monitored for the development of chest pain or heart rhythm irregularities during exercise.
While lifestyle changes may be enough treatment for some people with peripheral artery disease, others may require medication. Examples of medications used in treating peripheral artery disease include anti-platelet or anti-clotting agents, cholesterol-lowering drugs such as statins, medications that increase blood supply to the extremities such as cilostazol (Petal) and pentoxifylline (Trental), and medications that control high blood pressure.
Learn more about: Trental
Learn more about: Plavix
Learn more about: heparin | Coumadin
Learn more about: Pletal
Angioplasty is a non-surgical procedure that can widen a narrowed or blocked artery. A thin tube (catheter) is inserted into an artery in the groin or arm, and advanced to the area of narrowing. A tiny balloon on the tip of the catheter is then inflated to enlarge the narrowing in the artery. This procedure is also commonly performed to dilate narrowed areas in the coronary arteries that supply blood to the heart muscle.
Sometimes the catheter technique is used to insert a stent (a cylindrical wire mesh tube) into the affected area of the artery to keep the artery open. In other cases, thrombolytic medications (medications that dissolve blood clots) may be delivered to the blocked area via a catheter.
Angioplasty does not require general anesthesia and may be performed by an interventional radiologist., cardiologist, or vascular surgeon. Usually, a local anesthetic at the area of catheter insertion and a mild sedative are given. Major complications of angioplasty are rare, but can occur. These include damage to the artery or blood clot formation, excessive bleeding from the catheter insertion site, and abrupt vessel closure (blockage of the treated area occurring within 24 hours of the procedure).
Despite these risks, the overall incidence of complications is low and the benefits of angioplasty (no general anesthesia, no surgical incision, and the ability to return to normal activities within a couple of days) outweigh its risks. Usually a one-night hospital stay is required when angioplasty is performed.
Angioplasty is indicated when a patient has claudication that limits his or her activities and does not respond to exercise, medications, and lifestyle measures. Most doctors also recommend angioplasty when disease is very severe and there is a focal, localized narrowing that is accessible via catheter. If a patient is too ill to have surgery and has severe ischemia (decreased oxygen) that threatens loss of a limb, angioplasty may also be attempted.
Some cases of peripheral artery disease may be more difficult to treat by angioplasty. For example, blockages in multiple small arteries of the legs or blockages in extremely small vessels may not be treatable by this method.
Cryoplasty is a newer form of angioplasty in which freezing is used to open a narrowed artery. In this procedure, the balloon on the catheter is filled with liquid nitrous oxide, which freezes and destroys plaques within the artery.
Surgical treatment for peripheral artery disease involves either bypass surgery performed by a vascular surgeon or endarterectomy. Indications for surgical treatment of peripheral artery disease include lesions that, for anatomical reasons, may be difficult to treat by angioplasty. Examples include lesions covering long segments of a vessel, vessels with multiple narrowed areas, or long areas of narrowing. Bypass surgery involves using a vein from your body or a portion of synthetic vessel (known as grafts) to create a detour around the blockage. One end of the graft is sewn to the damaged artery above the blockage and the other end is sewn below the blocked area. Blood flow is then able to bypass the area of narrowing or blockage Bypass surgery is a major surgical procedure requiring general anesthesia and a hospital stay.
Endarterectomy is a procedure in which the surgeon cleans out plaque buildup inside the artery of the affected leg or arm.
Additional Heart Attack Prevention Series Information (related articles)
Coronary atherosclerosis is the hardening and narrowing of the arteries that supply blood to the heart muscle. Coronary atherosclerosis is the major cause of heart attacks. Heart attacks are the major cause of sudden unexpected death among otherwise healthy adults in the prime of their lives. Heart attacks are also a significant cause of heart failure (due to weakened heart muscle) in this country. Heart failure considerably decreases a person's longevity and quality of life. In dollar terms, coronary heart disease is costly. The total cost of coronary artery bypass surgery, coronary angioplasty and stenting, medications, and hospitalizations exceeds 50 billion dollars annually.
Coronary atherosclerosis, and hence heart attacks, are preventable. A person can significantly lower his or her risk of heart attack by lowering high blood pressure, controlling diabetes, stopping cigarette smoking, losing excess weight, exercising regularly, and lowering the levels of bad "LDL" cholesterol and increasing the level of the good "HDL" cholesterol in the blood. In recent years, other risk factors for coronary atherosclerosis have been identified. These include a high serum homocysteine level and certain subtypes of LDL cholesterol. The following is a comprehensive review of the causes of atherosclerosis and heart attacks, and the means for their treatment and prevention.
Atherosclerosis is a gradual process whereby hard cholesterol substances (plaques) are deposited in the walls of the arteries. Cholesterol plaques cause hardening of the artery walls and narrowing of the inner channel (lumen) of the artery. Arteries carry blood that is enriched with oxygen and nutrients to the vital organs such as the brain, heart, kidneys, and liver. Arteries also transport blood to other tissues such as the fingers, toes, nerves, bones, skin, and muscles. Healthy arteries can deliver an ample supply of blood to the organs and tissues. In contrast, arteries that are narrowed by atherosclerosis have difficulty delivering blood to the parts of the body they supply. For example, atherosclerosis of the arteries in the legs causes poor circulation in the lower extremities. Poor circulation in the lower extremities can lead to pain while walking or exercising, deficient wound healing, and/or leg ulcers. Atherosclerosis can also cause the complete blockage of an artery from a blood clot. This complete blockage interrupts oxygen supply and results in tissue injury or death. Thus, the blockage of an artery that furnishes blood to the brain can lead to a stroke (death of brain tissue). Likewise, the blockage of the arteries to the heart can result in a heart attack (death of heart muscle), also called myocardial infarction (MI).
Coronary atherosclerosis refers to the hardening and narrowing of the coronary arteries. The coronary arteries supply the blood that carries oxygen and nutrients to the heart muscle. When coronary arteries are narrowed or blocked by atherosclerosis, they cannot deliver an adequate amount of blood to the heart muscle. Disease caused by the lack of blood supply to heart muscle is called coronary heart disease (CHD). Coronary heart diseases include heart attacks, sudden unexpected death, chest pain (angina), abnormal heart rhythms, and heart failure due to weakening of the heart muscle.
Angina pectoris is chest pain or pressure that occurs when the oxygen supply to the heart muscle cannot keep up with oxygen consumption by the heart muscle. (Oxygen consumption by the heart muscle increases with physical exertion or excitement and decreases with rest and relaxation.) Most commonly, the inadequate supply of oxygen is due to narrowing of the coronary arteries by atherosclerosis. When coronary arteries are narrowed by more than 50% to 70%, the arteries cannot increase the supply of blood to the heart muscle during exertion or other periods of high oxygen demand. An insufficient supply of oxygen to the heart muscle causes chest pain (angina). Chest pain that occurs with exercise or exertion is called exertional angina.
A heart attack (myocardial infarction) is the death of heart muscle due to the sudden and complete blockage of a coronary artery by a blood clot. A coronary artery blockage usually occurs in arteries that contain cholesterol plaques. A plaque can rupture and initiate the formation of a blood clot next to it. A blood clot can completely block blood flow through a coronary artery and deprive the heart muscle of needed nutrients and oxygen. The heart muscle then dies, which produces a heart attack.
A heart attack can trigger the sudden onset of ventricular fibrillation. Ventricular fibrillation is a chaotic electrical rhythm of the heart that causes cardiac arrest (the heart stands still and ceases to pump blood). Ventricular fibrillation causes permanent brain damage and death unless a normal heartbeat can be restored within five minutes of its onset. Of the one million Americans who suffer heart attacks annually, approximately 400,000 of them die suddenly and unexpectedly from ventricular fibrillation before the victims can reach any medical assistance. For these people, the first sign of coronary heart disease is sudden, unexpected death.
Unlike angina, a heart attack results in permanent damage of the heart muscle. After a heart attack, the damaged portion of the heart is left with a scar. If the amount of heart muscle damage and the area of scarring are small, the performance of the heart as a pump will not be significantly impaired. However, repeated heart attacks or a heart attack with extensive heart muscle damage, can weaken the heart and cause heart failure. People with heart failure experience shortness of breath, tolerate exercise poorly, and lack vigor because their weakened heart muscle cannot pump enough blood to keep their bodies healthy and active.
Cerebral vascular disease is caused by the reduced supply of blood to the brain. Examples of cerebral vascular disease include ischemic strokes, hemorrhagic strokes, and transient ischemic attacks and are discussed below.
An ischemic stroke is the sudden and permanent death of brain cells that occurs when the flow of blood to a part of the brain is blocked and oxygen cannot be delivered to the brain. Depending on the part of the brain that is affected, strokes can result in weakness or paralysis of the arms, legs, and/or facial muscles, loss of vision or speech, and difficulty walking.
Ischemic strokes most commonly occur when clots form in small arteries within the brain (known as thrombosis of the artery) that have been previously narrowed by atherosclerosis. The resulting strokes are called lacunar strokes because they look like small lakes. In some cases, blood clots can obstruct a larger artery going to the brain, such as the carotid artery in the neck, causing more extensive brain damage than lacunar strokes.
A second less common type of ischemic stroke occurs when a piece of a clot breaks loose, for example, from the carotid artery or heart, travels through the arteries, and lodges in an artery within the brain. This type of stroke is referred to as an embolic stroke and occurs commonly as a result of an irregular heart rhythm such as atrial fibrillation, that causes blood clots to form within the heart.
A hemorrhagic stroke occurs when a blood vessel in the brain ruptures, and blood leaks into the surrounding brain tissue. A hemorrhagic stroke, like an ischemic stroke, causes the death of tissue by depriving the brain of blood and oxygen. The accumulation of blood from the hemorrhage also can put pressure on adjacent parts of the brain and damage them as well.
A subarachnoid hemorrhage is a rupture of a blood vessel that is located between the outer surface of the brain and the inside of the skull. The blood vessel at the point of rupture often has been weakened by the development of an aneurysm (an abnormal ballooning of the wall of the blood vessel). Subarachnoid hemorrhages usually cause a sudden, severe headache and often are complicated by additional neurological problems, such as paralysis, coma, and even death.
A transient ischemic attack (TIA) often is referred to as a mini-stroke. TIAs are caused by the temporary reduction in flow of blood (ischemia) to the brain and is most often caused by a clot that spontaneously forms in a carotid artery. Patients with TIA's often have narrowed (or, less often, ulcerated) carotid arteries due to atherosclerosis. TIAs typically last 2 to 30 minutes, although symptoms sometimes can last 24 hours and can produce problems with vision, dizziness, weakness of the arms or legs, and trouble speaking. A TIA is different from a stroke in that it does not cause permanent death of brain tissue. Without treatment, however, patients with TIAs are at high risk for having a stroke with permanent damage to the brain.
Although the coronary arteries are wide open at birth, the atherosclerosis process begins early in life. Between the ages of 10 and 20, "fatty streaks" are already being deposited on the inner lining of the coronary arteries. Over the years, some of these fatty streaks grow into larger cholesterol plaques that can protrude into the artery lumen and harden the artery walls. Many men and women between the ages of 20 and 30 typically are unaware that their coronary arteries are gradually accumulating cholesterol plaques. But by ages 40 to 50, many people have developed enough atherosclerosis to put them at risk for coronary heart disease.
Atherosclerosis prevention should start early, preferably during childhood and adolescence. Most scientists believe that preventing atherosclerosis is more effective than trying to reverse established blockages or getting rid of plaques in the arteries. Therefore, children and adolescents should be taught lifetime habits of regular exercise, avoidance of smoking, and good nutrition. Unfortunately, many Americans have not taken adequate steps to prevent atherosclerosis. Reasons for this failure include:
Well-known risk factors for coronary atherosclerosis and heart attacks are:
Less recognized but just as important risk factors for coronary atherosclerosis are:
One can help to prevent atherosclerosis and reduce heart attack risks by:
Learn more about: aspirin
Many of the measures that prevent coronary atherosclerosis also benefit other arteries such as carotid arteries and cerebral arteries (arteries that supply blood to the brain). Therefore, these measures also prevent strokes.
Renal refers to anything related to the kidneys. Renal arteries carry blood from the heart to the kidneys. They branch directly from the aorta (the main artery coming off the heart) on either side and extend to each kidney. These arteries take a very large volume of blood to the kidneys to be filtered.
The heart pumps out approximately 5 liters of blood per minute, and about 1-1.5 liters (25%) of the total volume of blood pumped by the heart passes through the kidneys every minute.
Renal artery stenosis (narrowing) is a decrease in the diameter of the renal arteries. The resulting restriction of blood flow to the kidneys may lead to impaired kidney function (renal failure) and high blood pressure (hypertension), referred to as renovascular hypertension, or RVHT ("reno" for kidney and "vascular" for blood vessel). Renal artery stenosis is a major cause of RVHT and accounts for 1%-10% of the 50 million cases of hypertension in the United States.
Renovascular hypertension occurs when the artery to one of the kidneys is narrowed (unilateral, or one-sided, stenosis), while renal failure occurs when the arteries to both kidneys are narrowed (bilateral, or two-sided, stenosis). The decreased blood flow to both kidneys increasingly impairs renal function.
The majority of renal artery stenosis is caused by atherosclerosis (hardening and narrowing of blood vessel wall from the inside) similar to the process that occurs in blood vessels in the heart and other parts of the body.
Risk factors for atherosclerosis include:
Less common causes of renal artery stenosis are fibromuscular dysplasia of the vessels (narrowing of the vessel due to internal thickening of the blood vessel wall), arteritis (inflammation of the blood vessel), or dissection (tearing and division of the blood vessel wall).
Narrowing of the kidney arteries is more common in individuals 50 years of age and older. It is estimated that some degree of narrowing (greater than 50%) is found in about 18% of adults between 65-75 years of age and 42% of those older than 75 years of age. This may be due to the fact that atherosclerosis is more common in this age group.
In younger patients, the narrowing of the renal artery usually is due to the thickening of the artery (fibromuscular dysplasia) and it is more common in women than men.
It is estimated that renal artery stenosis accounts for approximately 1% of mild to moderate cases of high blood pressure. It may be responsible for more than 10% of cases of severely elevated or difficult to treat high blood pressure (hypertension).
In general, renal artery stenosis is not associated with any obvious or specific symptoms. Suspicious signs for renal artery stenosis include:
Typically, unilateral (one-sided) renal artery stenosis may be related to high blood pressure whereas bilateral (two-sided) renal artery stenosis is more often related to diminished kidney function.
When the circulating blood volume becomes depleted as a result of, for example, dehydration or bleeding, the blood flow to the kidneys is likewise reduced. The normal physiologic reaction to a decrease in blood flow to the kidneys is a complex hormonal response by the kidneys, called the renin-angiotensin-aldosterone system.
This hormonal system is activated as a defense against low blood pressure and low circulating blood volume. The kidney senses a possible decrease in the circulating blood when blood flow through these vessels is reduced. As a result, there are increased blood levels of the hormone angiotensin 2, which causes narrowing of the small blood vessels in the kidneys.
This, together with increased blood aldosterone levels (another hormone), promotes salt retention by the kidneys, and works to maintain blood pressure and restore blood volume. Accordingly, this hormonal system is protective in response to reduced circulation of blood to the kidneys that is caused either by volume depletion, as described, or by reduced blood pressure.
This otherwise normal hormonal response can become abnormal (pathologic) when the decreased blood flow to the kidneys results from a narrowing of diseased renal arteries. In this situation, the kidneys receive less blood flow, which then signals a sense of depletion of the circulating blood volume, despite the fact that the blood volume is actually normal. So, the diminished renal blood flow, by stimulating the production of angiotensin 2 and aldosterone, can lead to an abnormal increase of blood pressure (renovascular hypertension).
A search for renal artery stenosis may be undertaken in patients with progressive kidney failure of unknown cause, or in individuals with difficult to treat high blood pressure (hypertension that does not respond well to medications). The diagnosis of renal artery stenosis may be considered when any or all of the following are present:
Several tests exist to detect any evidence of renal artery stenosis. They can be divided into imaging tests and functional tests. The imaging tests provide a picture of the blood vessel and its anatomy and reveal the degree of narrowing. The functional tests provide information about whether the narrowing is significant enough to cause the high blood pressure or kidney dysfunction. Each of these tests has advantages and shortcomings.
An angiogram of the renal arteries is the best test available to detect the degree of narrowing. This is similar to an angiogram of the heart and involves insertion of a catheter through the groin into the main artery (the aorta), that is advanced to the level of the renal arteries. A dye is injected, and x-ray images are taken to see the caliber of the blood vessel and extent of the narrowing.
An angiogram is considered an invasive test (insertion of the catheter inside the body) and therefore is not widely used because of the risk of complications. This test also may not determine if narrowing is truly significant to cause the problem or not, and so it may be necessary to combine this with a functional test. Generally, a narrowing of greater than 75% by angiogram is considered significant enough to cause high blood pressure or kidney dysfunction. An additional advantage of an angiogram is that if a treatable narrowing is seen, it may be fixed at the same time via angioplasty or by placing a stent (described in more detail below).
Other less invasive imaging tests are available to detect renal artery stenosis, but they are not generally as accurate as the angiogram and could potentially miss some cases of correctable disease. The most commonly used additional imaging tests are:
Magnetic resonance angiography (MRA) is similar to a magnetic resonance imaging (MRI). Contrast dye is injected into the blood via a vein in the arm, and pictures of the specific area of the body (in this case the renal arteries) are taken and analyzed. The accuracy (specificity and sensitivity) of this test is reasonable. This test cannot be done in patients with metal implants, pacemakers, or claustrophobia (fear of closed spaces). It may be used in people with mild to moderate, but not severe, kidney problems.
Computed tomographic angiography is similar to a computed tomography (CT scan) and has reasonable accuracy. This is also done by injecting a contrast dye into the blood and taking pictures of the renal arteries. This is not recommended in people with moderate to severe kidney problems as it may make the problem worse.
Doppler ultrasound is the least invasive imaging test for renal artery stenosis. It is performed similarly to a regular ultrasound by placing a probe on the abdomen to visualize the flow across the renal arteries and also to measure any narrowing. Its accuracy is similar to the other tests above, but its advantage is that it can measure the size of the narrowing as well as the flow across it. The disadvantage of this test is that it is time-consuming and may take up to a couple of hours to complete. It is also very operator-dependent, meaning that the accuracy of the result is dependent upon the expertise and experience of the ultrasound technician.
The main functional tests for renal artery stenosis include the plasma renin activity test and captopril renogram. These tests have been largely replaced by the imaging tests described above because they are less accurate, but they may be still performed to help establish the diagnosis of renal artery stenosis.
The plasma renin activity measures the activity of the hormone renin (described above). Activity of renin is generally higher in the kidney with renal artery stenosis compared to the other kidney. This response may be exaggerated by administration of captopril (Capoten), an ACE inhibitor medication used to treat high blood pressure.
Learn more about: Capoten
The renogram measures the activity of the kidneys after injection of a radioactive material that is taken up by the kidney. By administering captopril prior to the test, the activity may become more enhanced on the normal kidney compared to the one with renal artery stenosis. This may indicate a significant renal artery narrowing on the side with less activity.
In bilateral (both-sided) and unilateral (one-sided) renal artery stenosis associated with high blood pressure, controlling the blood pressure with usual blood pressure medications is the first and the safest treatment. ACE inhibitors or ARB medications with or without a diuretic (water pill) may be tried first. This approach may be associated in some patients with worsening of their kidney function. Therefore, kidney function needs to be followed closely and if worsening of kidney function is evident, these medications may need to be stopped.
It is worth noting that if renal artery stenosis is found incidentally when performing a test for another disease and there is no evidence of kidney dysfunction or high blood pressure, then no treatment may be necessary. Sometimes even significant stenosis may not be associated with high blood pressure or kidney dysfunction. In these situations, periodic monitoring of blood pressure and kidney function may be advised.
If the results of any of these screening tests suggest an abnormality of the renal artery, an x-ray angiography is then performed. A 75% or greater narrowing of the renal artery seen on the angiogram has been termed treatable renal artery stenosis.
Treatable means that the stenosis of the artery is severe (75% or greater narrowing), the artery needs to be widened (dilated), and it has a good chance of responding favorably to the dilatation. Usually right at the time of the angiography, an angioplasty is done. In this procedure a tiny balloon is inflated in the interior space in the artery (the lumen) to dilate the narrowed artery. Additionally, as part of the angioplasty procedure, a stent (tubular device to prevent recurrence of the narrowing) may be placed in the artery.
In rare cases, vascular surgery (on the blood vessels) may be done for renal artery stenosis. In these situations, typically another vascular surgery near the renal arteries, for example the aorta, is the main procedure. If renal artery stenosis is also present, then a bypass renal artery surgery may be done at the same time.
These invasive procedures are typically reserved for cases that do not respond to medical treatment and where it has been determined that the stenosis is causing or contributing to the uncontrolled high blood pressure. These invasive procedures may only be done if it is thought that the kidney dysfunction or elevated blood pressure can be effectively treated with the procedures.
In patients with renal failure due to bilateral renal artery stenosis (narrowing on both kidneys), angioplasty procedures for both renal arteries may improve or stabilize kidney function. Similarly, in hypertensive patients with unilateral (one-sided) renal artery stenosis, angioplasty procedures of the involved renal artery may cure or improve the high blood pressure. Patients with milder degrees of stenosis (less than a 75% reduction in the width of the renal artery lumen) usually do not benefit from angioplasty. These patients need to be followed by sequential imaging procedures to detect further narrowing (progression) to the point of treatable stenosis. At that point, angioplasty procedures can be done with the hope of a favorable response.
Some studies have suggested that patients with a very high degree of renal vascular resistance (which reflects permanent damage to the kidneys), even with a 75% or more stenosis of the renal artery, often have a poor response to the angioplasty procedures. (The tension of the blood vessels to the kidney, called renal vascular resistance, is measured by Doppler ultrasonography. A so-called resistive index over 0.8 is considered very high). In these patients, angioplasty is usually not done and the high blood pressure or renal failure is managed only by the customary therapeutic measures for these problems as described previously.
Jaundice can develop when red blood cells break down and bilirubin is left. It is normal for some red blood cells to die every day. In the womb, the mother's liver removes bilirubin for the baby, but after birth the baby's liver must remove the bilirubin. In some babies, the liver might not be developed enough to efficiently get rid of bilirubin. When too much bilirubin builds up in a new baby's body, the skin and whites of the eyes might look yellow. This yellow coloring is called jaundice.
Jaundice usually appears first on the face and then moves to the chest, belly, arms, and legs as bilirubin levels get higher. The whites of the eyes can also look yellow. Jaundice can be harder to see in babies with darker skin color. Your baby's doctor or nurse can test how much bilirubin is in your baby's blood.
About 60% of all babies have jaundice. Some babies are more likely to have severe jaundice and higher bilirubin levels than others. Babies with any of the following risk factors need close monitoring and early jaundice management:
Many babies have some jaundice. Jaundice can develop when red blood cells break down and bilirubin is left. It is normal for some red blood cells to die every day. In the womb, the mother's liver removes bilirubin for the baby, but after birth the baby's liver must remove the bilirubin. In some babies, the liver might not be developed enough to efficiently get rid of bilirubin. When too much bilirubin builds up in a new baby's body, the skin and whites of the eyes might look yellow. This yellow coloring is called jaundice. The yellow color does not hurt the baby's skin, but the bilirubin goes to the brain as well as to the skin. When severe jaundice goes untreated for too long, it can cause brain damage and a condition called kernicterus.
Kernicterus is a type of brain damage that causes athetoid cerebral palsy and hearing loss. It also causes problems with vision and teeth and sometimes can cause mental retardation.
Any baby with untreated jaundice is at risk for kernicterus. This does not mean that every baby with yellow skin will have brain damage. Most babies with jaundice get better by themselves. If their skin is very yellow, they might need phototherapy treatment. If phototherapy does not lower the baby's bilirubin levels, the baby may need an exchange transfusion.
Ask your pediatrician to see your baby the day you call, if your baby:
No baby should develop brain damage from untreated jaundice. If a baby gets too jaundiced, the baby can be treated with phototherapy. That is, the baby can be put under blue lights most of the day. The blue lights do not bother the baby. They are warm and probably feel good. If the baby gets very, very jaundiced, the doctor can do an exchange transfusion.
When being treated for high bilirubin levels, your baby will be undressed and put under special lights. The lights will not hurt the baby. This can be done in the hospital or at home. The baby's milk intake may also need to be increased. In some cases, if the baby has very high bilirubin levels, the doctor will do an exchange transfusion of the baby's blood. Jaundice is generally treated before brain damage is a concern. Putting your baby in sunlight is not recommended as a safe way of treating jaundice.
How do you measure bilirubin?
Before leaving the hospital with your newborn, ask your doctor or nurse about a jaundice bilirubin test.
A doctor or nurse may screen your baby's bilirubin using a light meter that is placed on the baby's head (as pictured). This results in a transcutaneous bilirubin (TcB) level. If it is high, a blood test will likely be ordered.
The best way to accurately measure bilirubin is with a small blood sample from the baby's heel.
This results in a total serum bilirubin (TSB) level. If the level is high, based upon the baby's age in hours and other risk factors, treatment will likely follow. Repeat blood samples will also likely be taken to ensure that the TSB decreases with the prescribed treatment.
If bilirubin levels are too high, what treatments are there?
Treatment for high levels of bilirubin will be ordered by your doctor or nurse.
Your baby is placed in contact with special lights that break down the bilirubin in the body. Phototherapy may be delivered through a blanket or light source around the baby's incubator or bassinet. This may be done in the hospital or at your home. Your doctor or nurse will prescribe the best form of treatment for your baby.
A blood transfusion may be needed if the bilirubin in your baby's body reaches extreme levels.
What does the term ringworm mean?
The term ringworm or ringworms refers to fungal infections that are on the surface of the skin. The name is derived from the early belief that the infection was due to a worm, which it is not. Ringworm is a fungal infection in the skin. Nevertheless, the name ringworm remains. Some of these fungi produce round spots on the skin, but many do not. On the other hand, many round, red spots on the skin are not due to a fungal infection. A physical examination of the affected skin, evaluation of skin scrapings under the microscope, and culture tests can help doctors make the appropriate distinctions. A proper diagnosis is essential to successful treatment.
The medical term for ringworm is tinea. (Tinea is the Latin name for a growing worm.) Doctors add another word to indicate where the fungus is located. Tinea capitis, for instance, refers to scalp ringworm, tinea corporis to fungus of the body, tinea pedis to fungus of the feet, and so on.
Ringworm occurs in people of all ages, but it is particularly common in children. Ringworm is contagious and can be passed from person to person by contact with infected skin areas or by sharing combs and brushes, other personal care items, or clothing. It is also possible become infected with ringworm after coming in contact with locker room or pool surfaces. The infection can also affect dogs and cats, who may transmit the infection to humans. It is common to have several areas of ringworm at once in different body areas.
Although the world is full of yeasts, molds, and fungi, only a few cause skin problems. These agents are called the dermatophytes, which means "skin fungi." An infection with these fungi is sometimes known as dermatophytosis. Skin fungi can only live on the dead layer of keratin protein on top of the skin. They rarely invade deeper into the body and cannot live on mucous membranes, such as those in the mouth or vagina.
Scientific names for the most common of the dermatophyte fungi that cause ringworm include Trichophyton rubrum, Trichophyton tonsurans, Trichophyton interdigitale, and/or Trichophyton mentagrophytes, Microsporum canis, and Epidermophyton floccosum.
Some fungi live only on human skin, hair, or nails. Others live on animals and only sometimes are found on human skin. Still others live in the soil. It is often difficult or impossible to identify the source of a particular person's skin fungus. The fungi may spread from person to person (anthropophilic), from animal to person (zoophilic), or from the soil to a person (geophilic).
Heat and moisture help fungi grow and thrive, which makes them more commonly found in skin folds such as those in the groin or between the toes. This also accounts for their reputation as being caught from showers, locker rooms, and swimming pools. This reputation is exaggerated, though, since many people with "jock itch" or "athlete's foot" have not contracted the infection from locker rooms or athletic facilities.
|What does ringworm look like?|
The following are the different types of ringworm, or tinea:
Often, the diagnosis of ringworm is obvious from its location and appearance. Otherwise, skin scrapings for microscopic examination and a culture of the affected skin can establish the diagnosis of ringworm. If the diagnosis is unclear, a potassium hydroxide (KOH) preparation of a skin scraping can be reviewed under the microscope to confirm the diagnosis of a fungal dermatophyte infection. If a dermatophyte infection is present and the skin problem is misdiagnosed, inappropriate treatment might be prescribed that could actually worsen the infection.
Antifungal medications are used to cure ringworm. Ringworm can be treated topically (with external applications) or systemically (for example, with oral medications):
Topical treatment: When fungus affects the skin of the body or the groin, many antifungal creams can clear the condition in around two weeks. Examples of such preparations include those that contain clotrimazole (Cruex cream, Desenex cream, Lotrimin cream, lotion, and solution), miconazole (Monistat-Derm cream), ketoconazole (Nizoral cream), econazole (Spectazole), naftifine (Naftin), and terbinafine (Lamisil cream and solution). These treatments are effective for many cases of foot fungus as well. Many of these antifungal creams are available as over-the-counter preparations. It is usually necessary to use topical medications for at least two weeks.
Learn more about: Monistat-Derm | Nizoral | Spectazole | Lamisil
Systemic treatment: Some fungal infections do not respond well to external applications. Examples include scalp fungus and fungus of the nails. To penetrate these areas and in cases of particularly severe or extensive disease, oral medications can be used.
For a long time, the only effective antifungal tablet was griseofulvin (Fulvicin, Grifulvin, and Gris-PEG). Now, other agents are available that are both safer and more effective. These include terbinafine, itraconazole (Sporanox), and fluconazole (Diflucan). Oral medications are usually given for a three-month course.
Conventional wisdom holds that minimizing sweat and moisture can help prevent fungal infections. Common recommendations along these lines are for men to wear boxer shorts, for women to avoid panty hose, and so forth. Whether these measures, some of which are quite difficult to implement, are really worth all of the effort is open to question.
You can also take steps to prevent transmission of ringworm infections. Do not share clothing, towels, hairbrushes, combs, hair accessories, or other personal care items. Wearing sandals or shoes in gyms, locker rooms, and at pools can help reduce your chances of contracting athlete's foot. You should avoid touching pets that have signs of ringworm (typically bald spots).
Athlete's foot is a very common skin infection of the bottom of the feet caused by fungus. The fungus that most commonly causes athlete's foot is called Trichophyton. When the feet or other areas of the body stay moist, warm, and become irritated, fungus can thrive and infect the upper layers of the skin. Fungal infections can occur almost anywhere on the body, including the scalp, trunk, extremities (arms and legs), hands, feet, nails, vagina, mouth, and groin.
Athlete's foot is caused by the ringworm fungus ("tinea" in medical jargon). Athlete's foot is also called tinea pedis. The fungus that causes athlete's foot can be found on many locations, including floors in gyms, locker rooms, swimming pools, nail salons, airport security lines, and in socks and clothing. The fungus can also be spread directly from person to person or by contact with these objects. Most people acquire fungus on the feet from walking barefoot on areas where someone else with athlete's foot has walked. Some people are simply more prone to this condition while others seem relatively resistant to contracting it. It has been called "jungle rot" by those serving in wars, including the Vietnam War.
However, without proper growing conditions (a warm, moist environment), the fungus may not easily infect the skin. Up to 70% of the population may have athlete's foot at some time during their lives. Some individuals are inherently more prone to recurrences during their lifetime.
Most individuals with athlete's foot have no symptoms at all and do not even know they have an infection. Many may think they simply have dry skin on the soles of their feet. Common symptoms of athlete's foot typically include various degrees of itching and burning. The skin may frequently peel, and in particularly severe cases, there may be some cracking, pain, and bleeding as well. Rarely, athlete's foot can blister (called bullous tinea pedis).
Most cases of athlete's foot are barely noticeable with just slightly dry, flaky skin. More extensive athlete's foot may look like red, peeling, dry skin areas on one or both soles of the feet. Sometimes the dry flakes may spread onto the sides and tops of the feet. Most commonly, the rash is localized to just the bottoms of the feet. The space between the fourth and fifth toes also may have some moisture, peeling, and dry flakes.
There are three common types of athlete's foot:
2. between the toes, also called "interdigital" type;
3. and inflammatory type or blistering.
Unusual cases may look like small or large blisters of the feet (called bullous tinea pedis), thick patches of dry, red skin, or calluses with redness. Sometimes, it may look like just mild dry skin without any redness or inflammation.
Athlete's foot may present as a rash on one or both feet and even involve the hand. A "two feet and one palm" presentation is a very common presentation of athlete's foot, especially in men. Hand fungal infections are called tinea manuum. The exact cause of why the infection commonly only affects one hand is not known.
Athlete's foot may also be seen along with ringworm of the groin (especially in men) or hand(s). It is helpful to examine the feet whenever there is a fungal groin rash called tinea cruris. It is important to treat all areas of fungal infection at one time to avoid re-infection. Simply treating the soles and ignoring the concurrent fungal infection of toenails may result in recurrences of athlete's foot. It is important to evaluate and address all potential sources of fungal infection.
Athlete's foot may be contagious from person to person, but it is not always contagious. Some people may be more susceptible to the fungus that causes athlete's foot while others are more resistant. There are many households where two people (often husband and wife or siblings) using the same showers and bathroom for years have not transmitted the fungus between them. The exact cause of this predisposition or susceptibility to fungal infections is unknown. Some people just seem more prone to fungal skin infections than others. Athlete's foot seems more contagious in moist, warm environments like public swimming pools, locker rooms, and yoga studio floors.
There are many possible causes of foot rashes. Athlete's foot is one of the more common causes. Additional causes include irritant or contact dermatitis, allergic rashes from shoes or other creams, dyshidrotic eczema (skin allergy rash), psoriasis, keratodermia blennorrhagicum, yeast infections, and bacterial infections.
Your physician can perform a simple test called a KOH, or potassium hydroxide for microscopic fungal examination, in the office or laboratory to confirm the presence of a fungal infection. This test is performed using small flakes of skin that are examined under the microscope. Many dermatologists perform this test in their office with results available within minutes. Rarely, a small piece of skin may be removed and sent for biopsy to help confirm the diagnosis.
The treatment of athlete's foot can be divided into two parts. The first, and most important part, is to make the infected area less suitable for the athlete's foot fungus to grow. This means keeping the area clean and dry.
Buy shoes that are leather or another breathable material. Shoe materials, such as vinyl, that don't breathe cause your feet to remain moist, providing an excellent area for the fungus to breed. Likewise, absorbent socks like cotton that wick water away from your feet may help.
Powders, especially medicated powders (such as with miconazole [Lotrimin] or tolnaftate [Tinactin]), can help keep your feet dry. Finally, your feet can be soaked in a drying solution of aluminum acetate (Burow's solution or Domeboro solution). A homemade remedy of dilute white vinegar soaks using 1 part vinegar and roughly 4 parts water, once or twice a day as 10-minute foot soaks may aid in treatment.
The second part of treatment is the use of antifungal creams and washes. Many medications are available, including miconazole, econazole nitrate (Spectazole), clotrimazole (Lotrimin), terbinafine (Lamisil) sprays and creams, and ketoconazole shampoo and cream (Nizoral), etc. Ask your health-care professional or pharmacist for a recommendation. Treatment for athlete's foot should generally be continued for four weeks or at least one week after all of the skin symptoms have cleared.
Learn more about: Spectazole | Lamisil | Nizoral
More advanced or resistant cases of athlete's foot may require a two- to three-week course of an oral (pill) antifungal like terbinafine (Lamisil), itraconazole (Sporanox), or fluconazole (Diflucan). Laboratory blood tests to make sure there is no liver disease may be required before taking these pills.
Topical corticosteroid creams can act as a fertilizer for fungus and may actually worsen fungal skin infections. These topical steroid medications have no role in treating athlete's foot.
If the fungal infection has spread to the toenails, the nails must also be treated to avoid re-infection of the feet. Often, the nails are initially ignored only to find the athlete's foot keeps recurring. It is important to treat all the visible fungus at the same time. Effective nail fungus treatment may be more intensive and require prolonged courses (three to four months) of oral antifungal medications.
Multiple home remedies are available including vinegar soaks, dilute Clorox soaks, and shampoos like Head & Shoulders or Selsun Blue. Other reported but unverified remedies have included Vicks Vapor Rub and Epsom salts.
Learn more about: Selsun
Treatment options during pregnancy may include dilute vinegar soaks or sprays (roughly 1 part white household vinegar to 4 parts water) and Lotrimin cream twice a day for two to three weeks to the soles. Antifungal pills are generally not recommended during pregnancy because of the potential side effects and possible fetal harm. Always check with your OB/GYN before using any medication or treatment during pregnancy.
If you notice any redness, increased swelling, bleeding, or if your infection is not clearing up, see your health-care practitioner. If a bacterial infection is also occurring, an antibiotic pill may be necessary. If you have fungal nail involvement, are diabetic, or have a compromised immune system, you should also see your physician for treatment.
Untreated, athlete's foot can potentially spread to other body parts or other people including family members. Fungus may spread locally to the legs, toenails, hands, fingernails, and essentially any body area.
This type of fungus generally likes to live in the skin, hair, and nails. It does not invade deep, go into body organs, or go into the blood system.
Fungal infections of the nails are called tinea unguium or onychomycosis. Nail fungus may be very difficult to treat. Antifungal pills may be required in cases of more advanced toenail fungal infections.
People with diabetes, HIV/AIDS, cancer, or other immune problems may be more prone to all kinds of infections, including fungus.
When the skin is injured by fungus, the natural protective skin barrier is broken. Bacteria and yeasts can then invade the broken skin. Bacteria can cause a bad smell. Bacterial infection of the skin and resulting inflammation is known as cellulitis. This is especially likely to occur those individuals with diabetes, chronic leg swelling, who have had veins removed (such as for heart bypass surgery), or in the elderly. Bacterial skin infections also occur more frequently in patients with impaired immune systems.
Dermatologists specialize in the treatment of skin disorders, including athlete's foot. You may find a board-certified dermatologist through http://www.aad.org. Additionally, family medicine physicians, internal medicine physicians, pediatricians, podiatrists (foot doctors), and other practitioners may also treat this common infection.
Since some people are simply more prone to fungal infections, they are also prone to repeated infection. Preventive measures include keeping your feet clean and dry, avoiding prolonged moist environments, using socks in airport security lines, removing shoes and allowing the feet skin to "breathe," avoiding walking barefoot, especially in public areas like swimming pools and gyms, avoiding contact with known infected people, and avoiding soaking and contaminated tool usage at nail salons. Disinfecting old shoes and periodic weekly or monthly sprinkling of antifungal foot powder (Pedi-Dry Foot Powder) into shoes can also be helpful.
It is imperative to take your own nail instruments, including nail files, to any public nail salon, unless you know the salon practices strict instrument sterilization and/or uses all disposable supplies.
Use cotton socks whenever possible. Avoid walking in airports and public areas with bare feet. Make sure any affected family members also treat their athlete's foot at the same time to avoid cross-infections.
Few experiences match the drama of a convulsive seizure. A person having a severe seizure may cry out, fall to the floor unconscious, twitch or move uncontrollably, drool, or even lose bladder control. Within minutes, the attack is over, and the person regains consciousness but is exhausted and dazed. This is the image most people have when they hear the word epilepsy. However, this type of seizure -- a generalized tonic-clonic seizure -- is only one kind of epilepsy. There are many other kinds, each with a different set of symptoms.
Epilepsy was one of the first brain disorders to be described. It was mentioned in ancient Babylon more than 3,000 years ago. The strange behavior caused by some seizures has contributed through the ages to many superstitions and prejudices. The word epilepsy is derived from the Greek word for "attack." People once thought that those with epilepsy were being visited by demons or gods. However, in 400 B.C., the early physician Hippocrates suggested that epilepsy was a disorder of the brain -- and we now know that he was right.
Epilepsy is a brain disorder in which clusters of nerve cells, or neurons, in the brain sometimes signal abnormally. Neurons normally generate electrochemical impulses that act on other neurons, glands, and muscles to produce human thoughts, feelings, and actions. In epilepsy, the normal pattern of neuronal activity becomes disturbed, causing strange sensations, emotions, and behavior, or sometimes convulsions, muscle spasms, and loss of consciousness. During a seizure, neurons may fire as many as 500 times a second, much faster than normal. In some people, this happens only occasionally; for others, it may happen up to hundreds of times a day.
More than 2 million people in the United States -- about 1 in 100 -- have experienced an unprovoked seizure or been diagnosed with epilepsy. For about 80 percent of those diagnosed with epilepsy, seizures can be controlled with modern medicines and surgical techniques. However, about 25 to 30 percent of people with epilepsy will continue to experience seizures even with the best available treatment. Doctors call this situation intractable epilepsy. Having a seizure does not necessarily mean that a person has epilepsy. Only when a person has had two or more seizures is he or she considered to have epilepsy.
Epilepsy is not contagious and is not caused by mental illness or mental retardation. Some people with mental retardation may experience seizures, but seizures do not necessarily mean the person has or will develop mental impairment. Many people with epilepsy have normal or above-average intelligence. Famous people who are known or rumored to have had epilepsy include the Russian writer Dostoyevsky, the philosopher Socrates, the military general Napoleon, and the inventor of dynamite, Alfred Nobel, who established the Nobel Prize. Several Olympic medalists and other athletes also have had epilepsy. Seizures sometimes do cause brain damage, particularly if they are severe. However, most seizures do not seem to have a detrimental effect on the brain. Any changes that do occur are usually subtle, and it is often unclear whether these changes are caused by the seizures themselves or by the underlying problem that caused the seizures.
While epilepsy cannot currently be cured, for some people it does eventually go away. One study found that children with idiopathic epilepsy, or epilepsy with an unknown cause, had a 68 to 92 percent chance of becoming seizure-free by 20 years after their diagnosis. The odds of becoming seizure-free are not as good for adults or for children with severe epilepsy syndromes, but it is nonetheless possible that seizures may decrease or even stop over time. This is more likely if the epilepsy has been well-controlled by medication or if the person has had epilepsy surgery.
Epilepsy is a disorder with many possible causes. Anything that disturbs the normal pattern of neuron activity -- from illness to brain damage to abnormal brain development -- can lead to seizures.
Epilepsy may develop because of an abnormality in brain wiring, an imbalance of nerve signaling chemicals called neurotransmitters, or some combination of these factors. Researchers believe that some people with epilepsy have an abnormally high level of excitatory neurotransmitters that increase neuronal activity, while others have an abnormally low level of inhibitory neurotransmitters that decrease neuronal activity in the brain. Either situation can result in too much neuronal activity and cause epilepsy. One of the most-studied neurotransmitters that plays a role in epilepsy is GABA, or gamma-aminobutyric acid, which is an inhibitory neurotransmitter. Research on GABA has led to drugs that alter the amount of this neurotransmitter in the brain or change how the brain responds to it. Researchers also are studying excitatory neurotransmitters such as glutamate.
In some cases, the brain's attempts to repair itself after a head injury, stroke, or other problem may inadvertently generate abnormal nerve connections that lead to epilepsy. Abnormalities in brain wiring that occur during brain development also may disturb neuronal activity and lead to epilepsy.
Research has shown that the cell membrane that surrounds each neuron plays an important role in epilepsy. Cell membranes are crucial for a neuron to generate electrical impulses. For this reason, researchers are studying details of the membrane structure, how molecules move in and out of membranes, and how the cell nourishes and repairs the membrane. A disruption in any of these processes may lead to epilepsy. Studies in animals have shown that, because the brain continually adapts to changes in stimuli, a small change in neuronal activity, if repeated, may eventually lead to full-blown epilepsy. Researchers are investigating whether this phenomenon, called kindling, may also occur in humans.
In some cases, epilepsy may result from changes in non-neuronal brain cells called glia. These cells regulate concentrations of chemicals in the brain that can affect neuronal signaling.
About half of all seizures have no known cause. However, in other cases, the seizures are clearly linked to infection, trauma, or other identifiable problems.
Research suggests that genetic abnormalities may be some of the most important factors contributing to epilepsy. Some types of epilepsy have been traced to an abnormality in a specific gene. Many other types of epilepsy tend to run in families, which suggests that genes influence epilepsy. Some researchers estimate that more than 500 genes could play a role in this disorder. However, it is increasingly clear that, for many forms of epilepsy, genetic abnormalities play only a partial role, perhaps by increasing a person's susceptibility to seizures that are triggered by an environmental factor.
Several types of epilepsy have now been linked to defective genes for ion channels, the "gates" that control the flow of ions in and out of cells and regulate neuron signaling. Another gene, which is missing in people with progressive myoclonus epilepsy, codes for a protein called cystatin B. This protein regulates enzymes that break down other proteins. Another gene, which is altered in a severe form of epilepsy called LaFora's disease, has been linked to a gene that helps to break down carbohydrates.
While abnormal genes sometimes cause epilepsy, they also may influence the disorder in subtler ways. For example, one study showed that many people with epilepsy have an abnormally active version of a gene that increases resistance to drugs. This may help explain why anticonvulsant drugs do not work for some people. Genes also may control other aspects of the body's response to medications and each person's susceptibility to seizures, or seizure threshold. Abnormalities in the genes that control neuronal migration -- a critical step in brain development -- can lead to areas of misplaced or abnormally formed neurons, or dysplasia, in the brain that can cause epilepsy. In some cases, genes may contribute to development of epilepsy even in people with no family history of the disorder. These people may have a newly developed abnormality, or mutation, in an epilepsy-related gene.
In many cases, epilepsy develops as a result of brain damage from other disorders. For example, brain tumors, alcoholism, and Alzheimer's disease frequently lead to epilepsy because they alter the normal workings of the brain. Strokes, heart attacks, and other conditions that deprive the brain of oxygen also can cause epilepsy in some cases. About 32 percent of all cases of newly developed epilepsy in elderly people appears to be due to cerebrovascular disease, which reduces the supply of oxygen to brain cells. Meningitis, AIDS, viral encephalitis, and other infectious diseases can lead to epilepsy, as can hydrocephalus -- a condition in which excess fluid builds up in the brain. Epilepsy also can result from intolerance to wheat gluten (also known as celiac disease), or from a parasitic infection of the brain called neurocysticercosis. Seizures may stop once these disorders are treated successfully. However, the odds of becoming seizure-free after the primary disorder is treated are uncertain and vary depending on the type of disorder, the brain region that is affected, and how much brain damage occurred prior to treatment.
Epilepsy is associated with a variety of developmental and metabolic disorders, including cerebral palsy, neurofibromatosis, pyruvate dependency, tuberous sclerosis, Landau-Kleffner syndrome, and autism. Epilepsy is just one of a set of symptoms commonly found in people with these disorders.
In some cases, head injury can lead to seizures or epilepsy. Safety measures such as wearing seat belts in cars and using helmets when riding a motorcycle or playing competitive sports can protect people from epilepsy and other problems that result from head injury.
Prenatal Injury and Developmental Problems
The developing brain is susceptible to many kinds of injury. Maternal infections, poor nutrition, and oxygen deficiencies are just some of the conditions that may take a toll on the brain of a developing baby. These conditions may lead to cerebral palsy, which often is associated with epilepsy, or they may cause epilepsy that is unrelated to any other disorders. About 20 percent of seizures in children are due to cerebral palsy or other neurological abnormalities. Abnormalities in genes that control development also may contribute to epilepsy. Advanced brain imaging has revealed that some cases of epilepsy that occur with no obvious cause may be associated with areas of dysplasia in the brain that probably develop before birth.
Seizures can result from exposure to lead, carbon monoxide, and many other poisons. They also can result from exposure to street drugs and from overdoses of antidepressants and other medications.
Seizures are often triggered by factors such as lack of sleep, alcohol consumption, stress, or hormonal changes associated with the menstrual cycle. These seizure triggers do not cause epilepsy but can provoke first seizures or cause breakthrough seizures in people who otherwise experience good seizure control with their medication. Sleep deprivation in particular is a universal and powerful trigger of seizures. For this reason, people with epilepsy should make sure to get enough sleep and should try to stay on a regular sleep schedule as much as possible. For some people, light flashing at a certain speed or the flicker of a computer monitor can trigger a seizure; this problem is called photosensitive epilepsy. Smoking cigarettes also can trigger seizures. The nicotine in cigarettes acts on receptors for the excitatory neurotransmitter acetylcholine in the brain, which increases neuronal firing. Seizures are not triggered by sexual activity except in very rare instances.
Doctors have described more than 30 different types of seizures. Seizures are divided into two major categories -- focal seizures and generalized seizures. However, there are many different types of seizures in each of these categories.
Focal seizures, also called partial seizures, occur in just one part of the brain. About 60 percent of people with epilepsy have focal seizures. These seizures are frequently described by the area of the brain in which they originate. For example, someone might be diagnosed with focal frontal lobe seizures.
In a simple focal seizure, the person will remain conscious but experience unusual feelings or sensations that can take many forms. The person may experience sudden and unexplainable feelings of joy, anger, sadness, or nausea. He or she also may hear, smell, taste, see, or feel things that are not real.
In a complex focal seizure, the person has a change in or loss of consciousness. His or her consciousness may be altered, producing a dreamlike experience. People having a complex focal seizure may display strange, repetitious behaviors such as blinks, twitches, mouth movements, or even walking in a circle. These repetitious movements are called automatisms. More complicated actions, which may seem purposeful, can also occur involuntarily. Patients may also continue activities they started before the seizure began, such as washing dishes in a repetitive, unproductive fashion. These seizures usually last just a few seconds.
Some people with focal seizures, especially complex focal seizures, may experience auras -- unusual sensations that warn of an impending seizure. These auras are actually simple focal seizures in which the person maintains consciousness. The symptoms an individual person has, and the progression of those symptoms, tend to be stereotyped, or similar every time.
The symptoms of focal seizures can easily be confused with other disorders. For instance, the dreamlike perceptions associated with a complex focal seizure may be misdiagnosed as migraine headaches, which also may cause a dreamlike state. The strange behavior and sensations caused by focal seizures also can be istaken for symptoms of narcolepsy, fainting, or even mental illness. It may take many tests and careful monitoring by an experienced physician to tell the difference between epilepsy and other disorders.
Generalized seizures are a result of abnormal neuronal activity on both sides of the brain. These seizures may cause loss of consciousness, falls, or massive muscle spasms.
There are many kinds of generalized seizures. In absence seizures, the person may appear to be staring into space and/or have jerking or twitching muscles. These seizures are sometimes referred to as petit mal seizures, which is an older term. Tonic seizures cause stiffening of muscles of the body, generally those in the back, legs, and arms. Clonic seizures cause repeated jerking movements of muscles on both sides of the body. Myoclonic seizures cause jerks or twitches of the upper body, arms, or legs. Atonic seizures cause a loss of normal muscle tone. The affected person will fall down or may drop his or her head involuntarily. Tonic-clonic seizures cause a mixture of symptoms, including stiffening of the body and repeated jerks of the arms and/or legs as well as loss of consciousness. Tonic-clonic seizures are sometimes referred to by an older term: grand mal seizures.
Not all seizures can be easily defined as either focal or generalized. Some people have seizures that begin as focal seizures but then spread to the entire brain. Other people may have both types of seizures but with no clear pattern.
Society's lack of understanding about the many different types of seizures is one of the biggest problems for people with epilepsy. People who witness a non-convulsive seizure often find it difficult to understand that behavior which looks deliberate is not under the person's control. In some cases, this has led to the affected person being arrested or admitted to a psychiatric hospital. To combat these problems, people everywhere need to understand the many different types of seizures and how they may appear.
Just as there are many different kinds of seizures, there are many different kinds of epilepsy. Doctors have identified hundreds of different epilepsy syndromes -- disorders characterized by a specific set of symptoms that include epilepsy. Some of these syndromes appear to be hereditary. For other syndromes, the cause is unknown. Epilepsy syndromes are frequently described by their symptoms or by where in the brain they originate. People should discuss the implications of their type of epilepsy with their doctors to understand the full range of symptoms, the possible treatments, and the prognosis.
People with absence epilepsy have repeated absence seizures that cause momentary lapses of consciousness. These seizures almost always begin in childhood or adolescence, and they tend to run in families, suggesting that they may be at least partially due to a defective gene or genes. Some people with absence seizures have purposeless movements during their seizures, such as a jerking arm or rapidly blinking eyes. Others have no noticeable symptoms except for brief times when they are "out of it." Immediately after a seizure, the person can resume whatever he or she was doing. However, these seizures may occur so frequently that the person cannot concentrate in school or other situations. Childhood absence epilepsy usually stops when the child reaches puberty. Absence seizures usually have no lasting effect on intelligence or other brain functions.
Temporal lobe epilepsy, or TLE, is the most common epilepsy syndrome with focal seizures. These seizures are often associated with auras. TLE often begins in childhood. Research has shown that repeated temporal lobe seizures can cause a brain structure called the hippocampus to shrink over time. The hippocampus is important for memory and learning. While it may take years of temporal lobe seizures for measurable hippocampal damage to occur, this finding underlines the need to treat TLE early and as effectively as possible.
Neocortical epilepsy is characterized by seizures that originate from the brain's cortex, or outer layer. The seizures can be either focal or generalized. They may include strange sensations, visual hallucinations, emotional changes, muscle spasms, convulsions, and a variety of other symptoms, depending on where in the brain the seizures originate.
There are many other types of epilepsy, each with its own characteristic set of symptoms. Many of these, including Lennox-Gastaut syndrome and Rasmussen's encephalitis, begin in childhood. Children with Lennox-Gastaut syndrome have severe epilepsy with several different types of seizures, including atonic seizures, which cause sudden falls and are also called drop attacks. This severe form of epilepsy can be very difficult to treat effectively. Rasmussen's encephalitis is a progressive type of epilepsy in which half of the brain shows continual inflammation. It sometimes is treated with a radical surgical procedure called hemispherectomy. Some childhood epilepsy syndromes, such as childhood absence epilepsy, tend to go into remission or stop entirely during adolescence, whereas other syndromes such as juvenile myoclonic epilepsy and Lennox-Gastaut syndrome are usually present for life once they develop. Seizure syndromes do not always appear in childhood, however.
Epilepsy syndromes that are easily treated, do not seem to impair cognitive functions or development, and usually stop spontaneously are often described as benign. Benign epilepsy syndromes include benign infantile encephalopathy and benign neonatal convulsions. Other syndromes, such as early myoclonic encephalopathy, include neurological and developmental problems. However, these problems may be caused by underlying neurodegenerative processes rather than by the seizures. Epilepsy syndromes in which the seizures and/or the person's cognitive abilities get worse over time are called progressive epilepsy.
Several types of epilepsy begin in infancy. The most common type of infantile epilepsy is infantile spasms, clusters of seizures that usually begin before the age of 6 months. During these seizures the infant may bend and cry out. Anticonvulsant drugs often do not work for infantile spasms, but the seizures can be treated with ACTH (adrenocorticotropic hormone) or prednisone.
While any seizure is cause for concern, having a seizure does not by itself mean a person has epilepsy. First seizures, febrile seizures, nonepileptic events, and eclampsia are examples of seizures that may not be associated with epilepsy.
Many people have a single seizure at some point in their lives. Often these seizures occur in reaction to anesthesia or a strong drug, but they also may be unprovoked, meaning that they occur without any obvious triggering factor. Unless the person has suffered brain damage or there is a family history of epilepsy or other neurological abnormalities, these single seizures usually are not followed by additional seizures. One recent study that followed patients for an average of 8 years found that only 33 percent of people have a second seizure within 4 years after an initial seizure. People who did not have a second seizure within that time remained seizure-free for the rest of the study. For people who did have a second seizure, the risk of a third seizure was about 73 percent on average by the end of 4 years.
When someone has experienced a first seizure, the doctor will usually order an electroencephalogram, or EEG, to determine what type of seizure the person may have had and if there are any detectable abnormalities in the person's brain waves. Thedoctor also may order brain scans to identify abnormalities that may be visible in the brain. These tests may help the doctor decide whether or not to treat the person with antiepileptic drugs. In some cases, drug treatment after the first seizure may help prevent future seizures and epilepsy. However, the drugs also can cause detrimental side effects, so doctors prescribe them only when they feel the benefits outweigh the risks. Evidence suggests that it may be beneficial to begin anticonvulsant medication once a person has had a second seizure, as the chance of future seizures increases significantly after this occurs.
Sometimes a child will have a seizure during the course of an illness with a high fever. These seizures are called febrile seizures (febrile is derived from the Latin word for "fever") and can be very alarming to the parents and other caregivers. In the past, doctors usually prescribed a course of anticonvulsant drugs following a febrile seizure in the hope of preventing epilepsy. However, most children who have a febrile seizure do not develop epilepsy, and long-term use of anticonvulsant drugs in children may damage the developing brain or cause other detrimental side effects. Experts at a 1980 consensus conference coordinated by the National Institutes of Health concluded that preventive treatment after a febrile seizure is generally not warranted unless certain other conditions are present: a family history of epilepsy, signs of nervous system impairment prior to the seizure, or a relatively prolonged or complicated seizure. The risk of subsequent non-febrile seizures is only 2 to 3 percent unless one of these factors is present.
Researchers have now identified several different genes that influence the risk of febrile seizures in certain families. Studying these genes may lead to new understanding of how febrile seizures occur and perhaps point to ways of preventing them.
Sometimes people appear to have seizures, even though their brains show no seizure activity. This type of phenomenon has various names, including nonepileptic events and pseudoseizures. Both of these terms essentially mean something that looks like a seizure but isn't one. Nonepileptic events that are psychological in origin may be referred to as psychogenic seizures. Psychogenic seizures may indicate dependence, a need for attention, avoidance of stressful situations, or specific psychiatric conditions. Some people with epilepsy have psychogenic seizures in addition to their epileptic seizures. Other people who have psychogenic seizures do not have epilepsy at all. Psychogenic seizures cannot be treated in the same way as epileptic seizures. Instead, they are often treated by mental health specialists.
Other nonepileptic events may be caused by narcolepsy, Tourette syndrome, cardiac arrythmia, and other medical conditions with symptoms that resemble seizures. Because symptoms of these disorders can look very much like epileptic seizures, they are often mistaken for epilepsy. Distinguishing between true epileptic seizures and nonepileptic events can be very difficult and requires a thorough medical assessment, careful monitoring, and knowledgeable health professionals. Improvements in brain scanning and monitoring technology may improve diagnosis of nonepileptic events in the future.
Eclampsia is a life-threatening condition that can develop in pregnant women. Its symptoms include sudden elevations of blood pressure and seizures. Pregnant women who develop unexpected seizures should be rushed to a hospital immediately. Eclampsia can be treated in a hospital setting and usually does not result in additional seizures or epilepsy once the pregnancy is over.
Doctors have developed a number of different tests to determine whether a person has epilepsy and, if so, what kind of seizures the person has. In some cases, people may have symptoms that look very much like a seizure but in fact are nonepileptic events caused by other disorders. Even doctors may not be able to tell the difference between these disorders and epilepsy without close observation and intensive testing.
An EEG records brain waves detected by electrodes placed on the scalp. This is the most common diagnostic test for epilepsy and can detect abnormalities in the brain's electrical activity. People with epilepsy frequently have changes in their normal pattern of brain waves, even when they are not experiencing a seizure. While this type of test can be very useful in diagnosing epilepsy, it is not foolproof. Some people continue to show normal brain wave patterns even after they have experienced a seizure. In other cases, the unusual brain waves are generated deep in the brain where the EEG is unable to detect them. Many people who do not have epilepsy also show some unusual brain activity on an EEG. Whenever possible, an EEG should be performed within 24 hours of a patient's first seizure. Ideally, EEGs should be performed while the patient is sleeping as well as when he or she is awake, because brain activity during sleep is often quite different than at other times.
Video monitoring is often used in conjunction with EEG to determine the nature of a person's seizures. It also can be used in some cases to rule out other disorders such as cardiac arrythmia or narcolepsy that may look like epilepsy.
One of the most important ways of diagnosing epilepsy is through the use of brain scans. The most commonly used brain scans include CT (computed tomography), PET (positron emission tomography) and MRI (magnetic resonance imaging). CT and MRI scans reveal the structure of the brain, which can be useful for identifying brain tumors, cysts, and other structural abnormalities. PET and an adapted kind of MRI called functional MRI (fMRI) can be used to monitor the brain's activity and detect abnormalities in how it works. SPECT (single photon emission computed tomography) is a relatively new kind of brain scan that is sometimes used to locate seizure foci in the brain.
In some cases, doctors may use an experimental type of brain scan called a magnetoencephalogram, or MEG. MEG detects the magnetic signals generated by neurons to allow doctors to monitor brain activity at different points in the brain over time, revealing different brain functions. While MEG is similar in concept to EEG, it does not require electrodes and it can detect signals from deeper in the brain than an EEG. Doctors also are experimenting with brain scans called magnetic resonance spectroscopy (MRS) that can detect abnormalities in the brain's biochemical processes, and with near-infrared spectroscopy, a technique that can detect oxygen levels in brain tissue.
Taking a detailed medical history, including symptoms and duration of the seizures, is still one of the best methods available to determine if a person has epilepsy and what kind of seizures he or she has. The doctor will ask questions about the seizures and any past illnesses or other symptoms a person may have had. Since people who have suffered a seizure often do not remember what happened, caregivers' accounts of the seizure are vital to this evaluation.
Doctors often take blood samples for testing, particularly when they are examining a child. These blood samples are often screened for metabolic or genetic disorders that may be associated with the seizures. They also may be used to check for underlying problems such as infections, lead poisoning, anemia, and diabetes that may be causing or triggering the seizures.
Developmental, Neurological, and Behavioral Tests
Doctors often use tests devised to measure motor abilities, behavior, and intellectual capacity as a way to determine how the epilepsy is affecting that person. These tests also can provide clues about what kind of epilepsy the person has.
Many cases of epilepsy can be prevented by wearing seatbelts and bicycle helmets, putting children in car seats, and other measures that prevent head injury and other trauma. Prescribing medication after first or second seizures or febrile seizures also may help prevent epilepsy in some cases. Good prenatal care, including treatment of high blood pressure and infections during pregnancy, can prevent brain damage in the developing baby that may lead to epilepsy and other neurological problems later. Treating cardiovascular disease, high blood pressure, infections, and other disorders that can affect the brain during adulthood and aging also may prevent many cases of epilepsy. Finally, identifying the genes for many neurological disorders can provide opportunities for genetic screening and prenatal diagnosis that may ultimately prevent many cases of epilepsy.
Accurate diagnosis of the type of epilepsy a person has is crucial for finding an effective treatment. There are many different ways to treat epilepsy. Currently available treatments can control seizures at least some of the time in about 80 percent of people with epilepsy. However, another 20 percent -- about 600,000 people with epilepsy in the United States -- have intractable seizures, and another 400,000 feel they get inadequate relief from available treatments. These statistics make it clear that improved treatments are desperately needed.
Doctors who treat epilepsy come from many different fields of medicine. They include neurologists, pediatricians, pediatric neurologists, internists, and family physicians, as well as neurosurgeons and doctors called epileptologists who specialize in treating epilepsy. People who need specialized or intensive care for epilepsy may be treated at large medical centers and neurology clinics at hospitals or by neurologists in private practice. Many epilepsy treatment centers are associated with university hospitals that perform research in addition to providing medical care.
Once epilepsy is diagnosed, it is important to begin treatment as soon as possible. Research suggests that medication and other treatments may be less successful in treating epilepsy once seizures and their consequences become established.
By far the most common approach to treating epilepsy is to prescribe antiepileptic drugs. The first effective antiepileptic drugs were bromides, introduced by an English physician named Sir Charles Locock in 1857. He noticed that bromides had a sedative effect and seemed to reduce seizures in some patients. More than 20 different antiepileptic drugs are now on the market, all with different benefits and side effects. The choice of which drug to prescribe, and at what dosage, depends on many different factors, including the type of seizures a person has, the person's lifestyle and age, how frequently the seizures occur, and, for a woman, the likelihood that she will become pregnant. People with epilepsy should follow their doctor's advice and share any concerns they may have regarding their medication.
Doctors seeing a patient with newly developed epilepsy often prescribe carbamazepine, valproate, lamotrigine, oxcarbazepine, or phenytoin first, unless the epilepsy is a type that is known to require a different kind of treatment. For absence seizures, ethosuximide is often the primary treatment. Other commonly prescribed drugs include clonazepam, phenobarbital, and primidone. Some relatively new epilepsy drugs include tiagabine, gabapentin, topiramate, levetiracetam, and felbamate. Other drugs are used in combination with one of the standard drugs or for intractable seizures that do not respond to other medications. A few drugs, such as fosphenytoin, are approved for use only in hospital settings to treat specific problems such as status epilepticus (see section, “Are There Special Risks Associated With Epilepsy?”). For people with stereotyped recurrent severe seizures that can be easily recognized by the person's family, the drug diazepam is now available as a gel that can be administered rectally by a family member. This method of drug delivery may be able to stop prolonged or repeated seizures before they develop into status epilepticus.
For most people with epilepsy, seizures can be controlled with just one drug at the optimal dosage. Combining medications usually amplifies side effects such as fatigue and decreased appetite, so doctors usually prescribe monotherapy, or the use of just one drug, whenever possible. Combinations of drugs are sometimes prescribed if monotherapy fails to effectively control a patient's seizures.
The number of times a person needs to take medication each day is usually determined by the drug's half-life, or the time it takes for half the drug dose to be metabolized or broken down into other substances in the body. Some drugs, such as phenytoin and phenobarbital, only need to be taken once a day, while others such as valproate must be taken two or three times a day.
Most side effects of antiepileptic drugs are relatively minor, such as fatigue, dizziness, or weight gain. However, severe and life-threatening side effects such as allergic reactions can occur. Epilepsy medication also may predispose people to developing depression or psychoses. People with epilepsy should consult a doctor immediately if they develop any kind of rash while on medication, or if they find themselves depressed or otherwise unable to think in a rational manner. Other danger signs that should be discussed with a doctor immediately are extreme fatigue, staggering or other movement problems, and slurring of words. People with epilepsy should be aware that their epilepsy medication can interact with many other drugs in potentially harmful ways. For this reason, people with epilepsy should always tell doctors who treat them which medications they are taking. Women also should know that some antiepileptic drugs can interfere with the effectiveness of oral contraceptives, and they should discuss this possibility with their doctors.
Since people can become more sensitive to medications as they age, they may need to have their blood levels of medication checked occasionally to see if the dose needs to be adjusted. The effects of a particular medication also sometimes wear off over time, leading to an increase in seizures if the dose is not adjusted. People should know that some citrus fruit, in particular grapefruit juice, may interfere with breakdown of many drugs. This can cause too much of the drug to build up in their bodies, often worsening the side effects.
People taking epilepsy medication should be sure to check with their doctor and/or seek a second medical opinion if their medication does not appear to be working or if it causes unexpected side effects.
Tailoring the dosage of antiepileptic drugs
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When a person starts a new epilepsy drug, it is important to tailor the dosage to achieve the best results. People's bodies react to medications in very different and sometimes unpredictable ways, so it may take some time to find the right drug at the right dose to provide optimal control of seizures while minimizing side effects. A drug that has no effect or very bad side effects at one dose may work very well at another dose. Doctors will usually prescribe a low dose of the new drug initially and monitor blood levels of the drug to determine when the best possible dose has been reached.
Generic versions are available for many antiepileptic drugs. The chemicals in generic drugs are exactly the same as in the brand-name drugs, but they may be absorbed or processed differently in the body because of the way they are prepared. Therefore, patients should always check with their doctors before switching to a generic version of their medication.
Some doctors will advise people with epilepsy to discontinue their antiepileptic drugs after 2 years have passed without a seizure. Others feel it is better to wait for 4 to 5 years. Discontinuing medication should always be done with a doctor's advice and supervision. It is very important to continue taking epilepsy medication for as long as the doctor prescribes it. People also should ask the doctor or pharmacist ahead of time what they should do if they miss a dose. Discontinuing medication without a doctor's advice is one of the major reasons people who have been seizure-free begin having new seizures. Seizures that result from suddenly stopping medication can be very serious and can lead to status epilepticus. Furthermore, there is some evidence that uncontrolled seizures trigger changes in neurons that can make it more difficult to treat the seizures in the future.
The chance that a person will eventually be able to discontinue medication varies depending on the person's age and his or her type of epilepsy. More than half of children who go into remission with medication can eventually stop their medication without having new seizures. One study showed that 68 percent of adults who had been seizure-free for 2 years before stopping medication were able to do so without having more seizures and 75 percent could successfully discontinue medication if they had been seizure-free for 3 years. However, the odds of successfully stopping medication are not as good for people with a family history of epilepsy, those who need multiple medications, those with focal seizures, and those who continue to have abnormal EEG results while on medication.
When seizures cannot be adequately controlled by medications, doctors may recommend that the person be evaluated for surgery. Surgery for epilepsy is performed by teams of doctors at medical centers. To decide if a person may benefit from surgery, doctors consider the type or types of seizures he or she has. They also take into account the brain region involved and how important that region is for everyday behavior. Surgeons usually avoid operating in areas of the brain that are necessary for speech, language, hearing, or other important abilities. Doctors may perform tests such as a Wada test (administration of the drug amobarbitol into the carotid artery) to find areas of the brain that control speech and memory. They often monitor the patient intensively prior to surgery in order to pinpoint the exact location in the brain where seizures begin. They also may use implanted electrodes to record brain activity from the surface of the brain. This yields better information than an external EEG.
A 1990 National Institutes of Health consensus conference on surgery for epilepsy concluded that there are three broad categories of epilepsy that can be treated successfully with surgery. These include focal seizures, seizures that begin as focal seizures before spreading to the rest of the brain, and unilateral multifocal epilepsy with infantile hemiplegia (such as Rasmussen's encephalitis). Doctors generally recommend surgery only after patients have tried two or three different medications without success, or if there is an identifiable brain lesion--a damaged or dysfunctional area--believed to cause the seizures.
A study published in 2000 compared surgery to an additional year of treatment with antiepileptic drugs in people with longstanding temporal lobe epilepsy. The results showed that 64 percent of patients receiving surgery became seizure-free, compared to 8 percent of those who continued with medication only. Because of this study and other evidence, the American Academy of Neurology (AAN) now recommends surgery for TLE when antiepileptic drugs are not effective. However, the study and the AAN guidelines do not provide guidance on how long seizures should occur, how severe they should be, or how many drugs should be tried before surgery is considered. A nationwide study is now underway to determine how soon surgery for TLE should be performed.
If a person is considered a good candidate for surgery and has seizures that cannot be controlled with available medication, experts generally agree that surgery should be performed as early as possible. It can be difficult for a person who has had years of seizures to fully re-adapt to a seizure-free life if the surgery is successful. The person may never have had an opportunity to develop independence, and he or she may have had difficulties with school and work that could have been avoided with earlier treatment. Surgery should always be performed with support from rehabilitation specialists and counselors who can help the person deal with the many psychological, social, and employment issues he or she may face.
While surgery can significantly reduce or even halt seizures for some people, it is important to remember that any kind of surgery carries some amount of risk (usually small). Surgery for epilepsy does not always successfully reduce seizures and it can result in cognitive or personality changes, even in people who are excellent candidates for surgery. Patients should ask their surgeon about his or her experience, success rates, and complication rates with the procedure they are considering.
Even when surgery completely ends a person's seizures, it is important to continue taking seizure medication for some time to give the brain time to re-adapt. Doctors generally recommend medication for 2 years after a successful operation to avoid new seizures.
Surgery to treat underlying conditions
In cases where seizures are caused by a brain tumor, hydrocephalus, or other conditions that can be treated with surgery, doctors may operate to treat these underlying conditions. In many cases, once the underlying condition is successfully treated, a person's seizures will disappear as well.
Surgery to remove a seizure focus
The most common type of surgery for epilepsy is removal of a seizure focus, or small area of the brain where seizures originate. This type of surgery, which doctors may refer to as a lobectomy or lesionectomy, is appropriate only for focal seizures that originate in just one area of the brain. In general, people have a better chance of becoming seizure-free after surgery if they have a small, well-defined seizure focus. Lobectomies have a 55-70 percent success rate when the type of epilepsy and the seizure focus is well-defined. The most common type of lobectomy is a temporal lobe resection, which is performed for people with temporal lobe epilepsy. Temporal lobe resection leads to a significant reduction or complete cessation of seizures about 70 - 90 percent of the time.
Multiple subpial transection
When seizures originate in part of the brain that cannot be removed, surgeons may perform a procedure called a multiple subpial transection. In this type of operation, which has been commonly performed since 1989, surgeons make a series of cuts that are designed to prevent seizures from spreading into other parts of the brain while leaving the person's normal abilities intact. About 70 percent of patients who undergo a multiple subpial transection have satisfactory improvement in seizure control.
Corpus callosotomy, or severing the network of neural connections between the right and left halves, or hemispheres, of the brain, is done primarily in children with severe seizures that start in one half of the brain and spread to the other side. Corpus callosotomy can end drop attacks and other generalized seizures. However, the procedure does not stop seizures in the side of the brain where they originate, and these focal seizures may even increase after surgery.
Hemispherectomy and hemispherotomy
These procedures remove half of the brain's cortex, or outer layer. They are used predominantly in children who have seizures that do not respond to medication because of damage that involves only half the brain, as occurs with conditions such as Rasmussen's encephalitis, Sturge-Weber syndrome, and hemimegencephaly. While this type of surgery is very radical and is performed only as a last resort, children often recover very well from the procedure, and their seizures usually cease altogether. With intense rehabilitation, they often recover nearly normal abilities. Since the chance of a full recovery is best in young children, hemispherectomy should be performed as early in a child's life as possible. It is rarely performed in children older than 13.
The vagus nerve stimulator was approved by the U.S. Food and Drug Administration (FDA) in 1997 for use in people with seizures that are not well-controlled by medication. The vagus nerve stimulator is a battery-powered device that is surgically implanted under the skin of the chest, much like a pacemaker, and is attached to the vagus nerve in the lower neck. This device delivers short bursts of electrical energy to the brain via the vagus nerve. On average, this stimulation reduces seizures by about 20 - 40 percent. Patients usually cannot stop taking epilepsy medication because of the stimulator, but they often experience fewer seizures and they may be able to reduce the dose of their medication. Side effects of the vagus nerve stimulator are generally mild but may include hoarseness, ear pain, a sore throat, or nausea. Adjusting the amount of stimulation can usually eliminate most side effects, although the hoarseness typically persists. The batteries in the vagus nerve stimulator need to be replaced about once every 5 years; this requires a minor operation that can usually be performed as an outpatient procedure.
Several new devices may become available for epilepsy in the future. Researchers are studying whether transcranial magnetic stimulation (TMS), a procedure which uses a strong magnet held outside the head to influence brain activity, may reduce seizures. They also hope to develop implantable devices that can deliver drugs to specific parts of the brain.
Studies have shown that, in some cases, children may experience fewer seizures if they maintain a strict diet rich in fats and low in carbohydrates. This unusual diet, called the ketogenic diet, causes the body to break down fats instead of carbohydrates to survive. This condition is called ketosis. One study of 150 children whose seizures were poorly controlled by medication found that about one-fourth of the children had a 90 percent or better decrease in seizures with the ketogenic diet, and another half of the group had a 50 percent or better decrease in their seizures. Moreover, some children can discontinue the ketogenic diet after several years and remain seizure-free. The ketogenic diet is not easy to maintain, as it requires strict adherence to an unusual and limited range of foods. Possible side effects include retarded growth due to nutritional deficiency and a buildup of uric acid in the blood, which can lead to kidney stones. People who try the ketogenic diet should seek the guidance of a dietician to ensure that it does not lead to serious nutritional deficiency.
Researchers are not sure how ketosis inhibits seizures. One study showed that a byproduct of ketosis called beta-hydroxybutyrate (BHB) inhibits seizures in animals. If BHB also works in humans, researchers may eventually be able to develop drugs that mimic the seizure-inhibiting effects of the ketogenic diet.
Other Treatment Strategies
Researchers are studying whether biofeedback -- a strategy in which individuals learn to control their own brain waves -- may be useful in controlling seizures. However, this type of therapy is controversial and most studies have shown discouraging results. Taking large doses of vitamins generally does not help a person's seizures and may even be harmful in some cases. But a good diet and some vitamin supplements, particularly folic acid, may help reduce some birth defects and medication-related nutritional deficiencies. Use of non-vitamin supplements such as melatonin is controversial and can be risky. One study showed that melatonin may reduce seizures in some children, while another found that the risk of seizures increased measurably with melatonin. Most non-vitamin supplements such as those found in health food stores are not regulated by the FDA, so their true effects and their interactions with other drugs are largely unknown
Most people with epilepsy lead outwardly normal lives. Approximately 80 percent can be significantly helped by modern therapies, and some may go months or years between seizures. However, the condition can and does affect daily life for people with epilepsy, their family, and their friends. People with severe seizures that resist treatment have, on average, a shorter life expectancy and an increased risk of cognitive impairment, particularly if the seizures developed in early childhood. These impairments may be related to the underlying conditions tha cause epilepsy or to epilepsy treatment rather than the epilepsy itself.
Behavior and Emotions
It is not uncommon for people with epilepsy, especially children, to develop behavioral and emotional problems. Sometimes these problems are caused by embarrassment or frustration associated with epilepsy. Other problems may result from bullying, teasing, or avoidance in school and other social settings. In children, these problems can be minimized if parents encourage a positive outlook and independence, do not reward negative behavior with unusual amounts of attention, and try to stay attuned to their child's needs and feelings. Families must learn to accept and live with the seizures without blaming or resenting the affected person. Counseling services can help families cope with epilepsy in a positive manner. Epilepsy support groups also can help by providing a way for people with epilepsy and their family members to share their experiences, frustrations, and tips for coping with the disorder.
People with epilepsy have an increased risk of poor self-esteem, depression, and suicide. These problems may be a reaction to a lack of understanding or discomfort about epilepsy that may result in cruelty or avoidance by other people. Many people with epilepsy also live with an ever-present fear that they will have another seizure.
Driving and Recreation
For many people with epilepsy, the risk of seizures restricts their independence, in particular the ability to drive. Most states and the District of Columbia will not issue a driver's license to someone with epilepsy unless the person can document that they have gone a specific amount of time without a seizure (the waiting period varies from a few months to several years). Some states make exceptions for this policy when seizures don't impair consciousness, occur only during sleep, or have long auras or other warning signs that allow the person to avoid driving when a seizure is likely to occur. Studies show that the risk of having a seizure-related accident decreases as the length of time since the last seizure increases. One study found that the risk of having a seizure-related motor vehicle accident is 93 percent less in people who wait at least 1 year after their last seizure before driving, compared to people who wait for shorter intervals.
The risk of seizures also restricts people's recreational choices. For instance, people with epilepsy should not participate in sports such as skydiving or motor racing where a moment's inattention could lead to injury. Other activities, such as swimming and sailing, should be done only with precautions and/or supervision. However, jogging, football, and many other sports are reasonably safe for a person with epilepsy. Studies to date have not shown any increase in seizures due to sports, although these studies have not focused on any activity in particular. There is some evidence that regular exercise may even improve seizure control in some people. Sports are often such a positive factor in life that it is best for the person to participate, although the person with epilepsy and the coach or other leader should take appropriate safety precautions. It is important to take steps to avoid potential sports-related problems such as dehydration, overexertion, and hypoglycemia, as these problems can increase the risk of seizures.
Education and Employment
By law, people with epilepsy or other handicaps in the United States cannot be denied employment or access to any educational, recreational, or other activity because of their seizures. However, one survey showed that only about 56 percent of people with epilepsy finish high school and about 15 percent finish college -- rates much lower than those for the general population. The same survey found that about 25 percent of working-age people with epilepsy are unemployed. These numbers indicate that significant barriers still exist for people with epilepsy in school and work. Restrictions on driving limit the employment opportunities for many people with epilepsy, and many find it difficult to face the misunderstandings and social pressures they encounter in public situations. Antiepileptic drugs also may cause side effects that interfere with concentration and memory. Children with epilepsy may need extra time to complete schoolwork, and they sometimes may need to have instructions or other information repeated for them. Teachers should be told what to do if a child in their classroom has a seizure, and parents should work with the school system to find reasonable ways to accommodate any special needs their child may have.
Pregnancy and Motherhood
Women with epilepsy are often concerned about whether they can become pregnant and have a healthy child. This is usually possible. While some seizure medications and some types of epilepsy may reduce a person's interest in sexual activity, most people with epilepsy can become pregnant. Moreover, women with epilepsy have a 90 percent or better chance of having a normal, healthy baby, and the risk of birth defects is only about 4 to 6 percent. The risk that children of parents with epilepsy will develop epilepsy themselves is only about 5 percent unless the parent has a clearly hereditary form of the disorder. Parents who are worried that their epilepsy may be hereditary may wish to consult a genetic counselor to determine what the risk might be. Amniocentesis and high-level ultrasound can be performed during pregnancy to ensure that the baby is developing normally, and a procedure called a maternal serum alpha-fetoprotein test can be used for prenatal diagnosis of many conditions if a problem is suspected.
There are several precautions women can take before and during pregnancy to reduce the risks associated with pregnancy and delivery. Women who are thinking about becoming pregnant should talk with their doctors to learn any special risks associated with their epilepsy and the medications they may be taking. Some seizure medications, particularly valproate, trimethidone, and phenytoin, are known to increase the risk of having a child with birth defects such as cleft palate, heart problems, or finger and toe defects. For this reason, a woman's doctor may advise switching to other medications during pregnancy. Whenever possible, a woman should allow her doctor enough time to properly change medications, including phasing in the new medications and checking to determine when blood levels are stabilized, before she tries to become pregnant. Women should also begin prenatal vitamin supplements -- especially with folic acid, which may reduce the risk of some birth defects -- well before pregnancy. Women who discover that they are pregnant but have not already spoken with their doctor about ways to reduce the risks should do so as soon as possible. However, they should continue taking seizure medication as prescribed until that time to avoid preventable seizures. Seizures during pregnancy can harm the developing baby or lead to miscarriage, particularly if the seizures are severe. Nevertheless, many women who have seizures during pregnancy have normal, healthy babies.
Women with epilepsy sometimes experience a change in their seizure frequency during pregnancy, even if they do not change medications. About 25 to 40 percent of women have an increase in their seizure frequency while they are pregnant, while other women may have fewer seizures during pregnancy. The frequency of seizures during pregnancy may be influenced by a variety of factors, including the woman's increased blood volume during pregnancy, which can dilute the effect of medication. Women should have their blood levels of seizure medications monitored closely during and after pregnancy, and the medication dosage should be adjusted accordingly.
Pregnant women with epilepsy should take prenatal vitamins and get plenty of sleep to avoid seizures caused by sleep deprivation. They also should take vitamin K supplements after 34 weeks of pregnancy to reduce the risk of a blood-clotting disorder in infants called neonatal coagulopathy that can result from fetal exposure to epilepsy medications. Finally, they should get good prenatal care, avoid tobacco, caffeine, alcohol, and illegal drugs, and try to avoid stress.
Labor and delivery usually proceed normally for women with epilepsy, although there is a slightly increased risk of hemorrhage, eclampsia, premature labor, and cesarean section. Doctors can administer antiepileptic drugs intravenously and monitor blood levels of anticonvulsant medication during labor to reduce the risk that the labor will trigger a seizure. Babies sometimes have symptoms of withdrawal from the mother's seizure medication after they are born, but these problems wear off in a few weeks or months and usually do not cause serious or long-term effects. A mother's blood levels of anticonvulsant medication should be checked frequently after delivery as medication often needs to be decreased.
Epilepsy medications need not influence a woman's decision about breast-feeding her baby. Only minor amounts of epilepsy medications are secreted in breast milk, usually not enough to harm the baby and much less than the baby was exposed to in the womb. On rare occasions, the baby may become excessively drowsy or feed poorly, and these problems should be closely monitored. However, experts believe the benefits of breast-feeding outweigh the risks except in rare circumstances.
To increase doctors' understanding of how different epilepsy medications affect pregnancy and the chances of having a healthy baby, Massachusetts General Hospital has begun a nationwide registry for women who take antiepileptic drugs while pregnant. Women who enroll in this program are given educational materials on pre-conception planning and perinatal care and are asked to provide information about the health of their children (this information is kept confidential). Women and physicians can contact this registry by calling 1-888-233-2334 or 617-726-1742 (fax: 617-724-8307).
Women with epilepsy should be aware that some epilepsy medications can interfere with the effectiveness of oral contraceptives. Women who wish to use oral contraceptives to prevent pregnancy should discuss this with their doctors, who may be able to prescribe a different kind of antiepileptic medication or suggest other ways of avoiding an unplanned pregnancy.
Although most people with epilepsy lead full, active lives, they are at special risk for two life-threatening conditions: status epilepticus and sudden unexplained death.
Status epilepticus is a potentially life-threatening condition in which a person either has an abnormally prolonged seizure or does not fully regain consciousness between seizures. Although there is no strict definition for the time at which a seizure turns into status epilepticus, most people agree that any seizure lasting longer than 5 minutes should, for practical purposes, be treated as though it was status epilepticus.
Status epilepticus affects about 195,000 people each year in the United States and results in about 42,000 deaths. While people with epilepsy are at an increased risk for status epilepticus, about 60 percent of people who develop this condition have no previous seizure history. These cases often result from tumors, trauma, or other problems that affect the brain and may themselves be life-threatening.
While most seizures do not require emergency medical treatment, someone with a prolonged seizure lasting more than 5 minutes may be in status epilepticus and should be taken to an emergency room immediately. It is important to treat a person with status epilepticus as soon as possible. One study showed that 80 percent of people in status epilepticus who received medication within 30 minutes of seizure onset eventually stopped having seizures, whereas only 40 percent recovered if 2 hours had passed before they received medication. Doctors in a hospital setting can treat status epilepticus with several different drugs and can undertake emergency life-saving measures, such as administering oxygen, if necessary.
People in status epilepticus do not always have severe convulsive seizures. Instead, they may have repeated or prolonged nonconvulsive seizures. This type of status epilepticus may appear as a sustained episode of confusion or agitation in someone who does not ordinarily have that kind of mental impairment. While this type of episode may not seem as severe as convulsive status epilepticus, it should still be treated as an emergency.
Sudden Unexplained Death
For reasons that are poorly understood, people with epilepsy have an increased risk of dying suddenly for no discernible reason. This condition, called sudden unexplained death, can occur in people without epilepsy, but epilepsy increases the risk about two-fold. Researchers are still unsure why sudden unexplained death occurs. One study suggested that use of more than two anticonvulsant drugs may be a risk factor. However, it is not clear whether the use of multiple drugs causes the sudden death, or whether people
While research has led to many advances in understanding and treating epilepsy, there are many unanswered questions about how and why seizures develop, how they can best be treated or prevented, and how they influence other brain activity and brain development. Researchers, many of whom are supported by the National Institute of Neurological Disorders and Stroke (NINDS), are studying all of these questions. They also are working to identify and test new drugs and other treatments for epilepsy and to learn how those treatments affect brain activity and development.
The NINDS's Anticonvulsant Screening Program (ASP) studies potential new therapies with the goal of enhancing treatment for patients with epilepsy. Since it began in 1975, more than 390 public-private partnerships have been created. These partnerships have resulted in state-of-the-art evaluations of more than 25,000 compounds for their potential as antiepileptic drugs. This government-sponsored effort has contributed to the development of five drugs that are now approved for use in the United States. It has also aided in the discovery and profiling of six new compounds currently in various stages of clinical development. Besides testing for safer, more efficacious therapies, the Program is developing and validating new models that may one day find therapies that intervene in the disease process itself as well as models of resistant or refractory epilepsy.
Scientists continue to study how excitatory and inhibitory neurotransmitters interact with brain cells to control nerve firing. They can apply different chemicals to cultures of neurons in laboratory dishes to study how those chemicals influence neuronal activity. They also are studying how glia and other non-neuronal cells in the brain contribute to seizures. This research may lead to new drugs and other new ways of treating seizures.
Researchers also are working to identify genes that may influence epilepsy in some way. Identifying these genes can reveal the underlying chemical processes that influence epilepsy and point to new ways of preventing or treating this disorder. Researchers also can study rats and mice that have missing or abnormal copies of certain genes to determine how these genes affect normal brain development and resistance to damage from disease and other environmental factors. In the future, researchers may be able to use panels of gene fragments, called "gene chips," to determine each person's genetic makeup. This information may allow doctors to prevent epilepsy or to predict which treatments will be most beneficial.
Doctors are now experimenting with several new types of therapies for epilepsy. In one preliminary clinical trial, doctors have begun transplanting fetal pig neurons that produce GABA into the brains of patients to learn whether the cell transplants can help control seizures. Preliminary research suggests that stem cell transplants also may prove beneficial for treating epilepsy. Research showing that the brain undergoes subtle changes prior to a seizure has led to a prototype device that may be able to predict seizures up to 3 minutes before they begin. If this device works, it could greatly reduce the risk of injury from seizures by allowing people to move to a safe area before their seizures start. This type of device also may be hooked up to a treatment pump or other device that will automatically deliver an antiepileptic drug or an electric impulse to forestall the seizures.
Researchers are continually improving MRI and other brain scans. Pre-surgical brain imaging can guide doctors to abnormal brain tissue and away from essential parts of the brain. Researchers also are using brain scans such as magnetoencephalograms (MEG) and magnetic resonance spectroscopy (MRS) to identify and study subtle problems in the brain that cannot otherwise be detected. Their findings may lead to a better understanding of epilepsy and how it can be treated.
There are many ways that people with epilepsy and their families can help with research on this disorder. Pregnant women with epilepsy who are taking antiepileptic drugs can help researchers learn how these drugs affect unborn children by participating in the Antiepileptic Drug Pregnancy Registry, which is maintained by the Genetics and Teratology Unit of Massachusetts General Hospital (see section on Pregnancy and Motherhood). People with epilepsy that may be hereditary can aid research by participating in the Epilepsy Gene Discovery Project, which is supported by the Epilepsy Foundation. This project helps to educate people with epilepsy about new genetic research on the disorder and enlists families with hereditary epilepsy for participation in gene research. People who enroll in this project are asked to create a family tree showing which people in their family have or have had epilepsy. Researchers then examine this information to determine if the epilepsy is in fact hereditary, and they may invite participants to enroll in genetic research studies. In many cases, identifying the gene defect responsible for epilepsy in an individual family leads researchers to new clues about how epilepsy develops. It also can provide opportunities for early diagnosis and genetic screening of individuals in the family.
People with epilepsy can help researchers test new medications, surgical techniques, and other treatments by enrolling in clinical trials. Information on clinical trials can be obtained from the NINDS as well as many private pharmaceutical and biotech companies, universities, and other organizations. A person who wishes to participate in a clinical trial must ask his or her regular physician to refer him or her to the doctor in charge of that trial and to forward all necessary medical records. While experimental therapies may benefit those who participate in clinical trials, patients and their families should remember that all clinical trials also involve some risks. Therapies being tested in clinical trials may not work, and in some cases doctors may not yet be sure that the therapies are safe. Patients should be certain they understand the risks before agreeing to participate in a clinical trial.
Patients and their families also can help epilepsy research by donating their brain to a brain bank after death. Brain banks supply researchers with tissue they can use to study epilepsy and other disorders. Below are some brain banks that accept tissue from patients with epilepsy:
If you see someone having a seizure with convulsions and/or loss of consciousness, here's how you can help:
Call 911 if:
Many people with epilepsy lead productive and outwardly normal lives. Medical and research advances in the past two decades have led to a better understanding of epilepsy and seizures than ever before. Advanced brain scans and other techniques allow greater accuracy in diagnosing epilepsy and determining when a patient may be helped by surgery. More than 20 different medications and a variety of surgical techniques are now available and provide good control of seizures for most people with epilepsy. Other treatment options include the ketogenic diet and the first implantable device, the vagus nerve stimulator. Research on the underlying causes of epilepsy, including identification of genes for some forms of epilepsy and febrile seizures, has led to a greatly improved understanding of epilepsy that may lead to more effective treatments or even new ways of preventing epilepsy in the future.
Eczema is a general term for many types of skin inflammation (dermatitis). The most common form of eczema is atopic dermatitis (sometimes these two terms are used interchangeably). However, there are many different forms of eczema.
Eczema can affect people of any age, although the condition is most common in infants, and about 85% of those affected have an onset prior to 5 years of age. Eczema will permanently resolve by age 3 in about half of affected infants. In others, the condition tends to recur throughout life. People with eczema often have a family history of the condition or a family history of other allergic conditions, such as asthma or hay fever. The nature of the link between these conditions is inadequately understood. Up to 20% of children and 1%-2% of adults are believed to have eczema. Eczema is slightly more common in girls than in boys. It occurs in people of all races.
Eczema is not contagious, but since it is believed to be at least partially inherited, it is not uncommon to find members of the same family affected.
Doctors do not know the exact cause of eczema, but a defect of the skin that impairs its function as a barrier, possibly combined with an abnormal function of the immune system, are believed to be important factors. Studies have shown that in people with atopic dermatitis there are gene defects that lead to abnormalities in certain proteins (such as filaggrin) that are important in maintaining the barrier of normal skin.
Some forms of eczema can be triggered by substances that come in contact with the skin, such as soaps, cosmetics, clothing, detergents, jewelry, or sweat. Environmental allergens (substances that cause allergic reactions) may also cause outbreaks of eczema. Changes in temperature or humidity, or even psychological stress, can lead to outbreaks of eczema in some people.
Eczema most commonly causes dry, reddened skin that itches or burns, although the appearance of eczema varies from person to person and varies according to the specific type of eczema. Intense itching is generally the first symptom in most people with eczema. Sometimes, eczema may lead to blisters and oozing lesions, but eczema can also result in dry and scaly skin. Repeated scratching may lead to thickened, crusty skin.
While any region of the body may be affected by eczema, in children and adults, eczema typically occurs on the face, neck, and the insides of the elbows, knees, and ankles. In infants, eczema typically occurs on the forehead, cheeks, forearms, legs, scalp, and neck.
Eczema can sometimes occur as a brief reaction that only leads to symptoms for a few hours or days, but in other cases, the symptoms persist over a longer time and are referred to as chronic dermatitis.
Atopic dermatitis is the most common of the many types of eczema, and sometimes people use the two terms interchangeably. But there are many terms used to describe specific forms of eczema that may have very similar symptoms to atopic dermatitis. These are listed and briefly described below.
Atopic dermatitis is a chronic skin disease characterized by itchy, inflamed skin and is the most common cause of eczema. The condition tends to come and go, depending upon exposures to triggers or causative factors. Factors that may cause atopic dermatitis (allergens) include environmental factors like molds, pollen, or pollutants; contact irritants like soaps, detergents, nickel (in jewelry), or perfumes; food allergies; or other allergies. Around two-thirds of those who develop the condition do so prior to 1 year of age. When the disease starts in infancy, it is sometimes termed infantile eczema. Atopic dermatitis tends to run in families, and people who develop the condition often have a family history of other allergic conditions such as asthma or hay fever.
Contact eczema (contact dermatitis) is a localized reaction that includes redness, itching, and burning in areas where the skin has come into contact with an allergen (an allergy-causing substance to which an individual is sensitized) or with a general irritant such as an acid, a cleaning agent, or other chemical. Other examples of contact eczema include reactions to laundry detergents, soaps, nickel (present in jewelry), cosmetics, fabrics, clothing, and perfume. Due to the vast number of substances with which individuals have contact, it can be difficult to determine the trigger for contact dermatitis. The condition is sometimes referred to as allergic contact eczema (allergic contact dermatitis) if the trigger is an allergen and irritant contact eczema (irritant contact dermatitis) if the trigger is an irritant. Skin reactions to poison ivy and poison sumac are examples of allergic contact eczema. People who have a history of allergies have an increased risk for developing contact eczema.
Seborrheic eczema (seborrheic dermatitis) is a form of skin inflammation of unknown cause. The signs and symptoms of seborrheic eczema include yellowish, oily, scaly patches of skin on the scalp, face, and occasionally other parts of the body. Dandruff and "cradle cap" in infants are examples of seborrheic eczema. It is commonplace for seborrheic dermatitis to inflame the face at the creases of the cheeks and/or the nasal folds. Seborrheic dermatitis is not necessarily associated with itching. This condition tends to run in families. Emotional stress, oily skin, infrequent shampooing, and weather conditions may all increase a person's risk of developing seborrheic eczema. One type of seborrheic eczema is also common in people with AIDS.
Nummular eczema (nummular dermatitis) is characterized by coin-shaped patches of irritated
Neurodermatitis, also known as lichen simplex chronicus, is a chronic skin inflammation caused by a scratch-itch cycle that begins with a localized itch (such as an insect bite) that becomes intensely irritated when scratched. Women are more commonly affected by neurodermatitis than men, and the condition is most frequent in people 20-50 years of age. This form of eczema results in scaly patches of skin on the head, lower legs, wrists, or forearms. Over time, the skin can become thickened and leathery. Stress can exacerbate the symptoms of neurodermatitis.
Stasis dermatitis is a skin irritation on the lower legs, generally related to the circulatory problem known as venous insufficiency, in which the function of the valves within the veins has been compromised. Stasis dermatitis occurs almost exclusively in middle-aged and elderly people, with approximately 6%-7% of the population over 50 years of age being affected by the condition. The risk of developing stasis dermatitis increases with advancing age. Symptoms include itching and/or reddish-brown discoloration of the skin on one or both legs. Progression of the condition can lead to the blistering, oozing skin lesions seen with other forms of eczema, and ulcers may develop in affected areas. The chronic circulatory problems lead to an increase in fluid buildup (edema) in the legs. Stasis dermatitis has also been referred to as varicose eczema.
Dyshidrotic eczema (dyshidrotic dermatitis) is an irritation of the skin on the palms of hands and soles of the feet characterized by clear, deep blisters that itch and burn. The cause of dyshidrotic eczema is unknown. Dyshidrotic eczema is also known as vesicular palmoplantar dermatitis, dyshidrosis, or pompholyx. This form of eczema occurs in up to 20% of people with hand eczema and is more common during the spring and summer months and in warmer climates. Males and females are equally affected, and the condition can occur in people of any age.
To diagnose eczema, doctors rely on a thorough physical examination of the skin as well as the patient's account of the history of the condition. In particular, the doctor will ask when the condition appeared, if the condition is associated with any changes in environment or contact with certain materials, and whether it is aggravated in any specific situations. Eczema may have a similar appearance to other diseases of the skin, including infections or reactions to certain medications, so the diagnosis is not always simple. In some cases, a biopsy of the skin may be taken in order to rule out other skin diseases that may be producing signs and symptoms similar to eczema.
If a doctor suspects that a patient has allergic contact dermatitis, allergy tests, possibly including a skin "patch test," may be carried out in an attempt to identify the specific trigger of the condition.
There are no laboratory or blood tests that can be used to establish the diagnosis of eczema.
The goals for the treatment of eczema are to prevent itching, inflammation, and worsening of the condition. Treatment of eczema may involve both lifestyle changes and the use of medications. Treatment is always based upon an individual's age, overall health status, and the type and severity of the condition.
Keeping the skin well hydrated through the application of creams or ointments (with a low water and high oil content) as well as avoiding over-bathing (see "Can eczema be prevented?" section) is an important step in treatment. It is recommended to apply emollient creams such as petrolatum-based creams to the body immediately after a five-minute lukewarm bath in order to seal in moisture while the body is still wet. Lifestyle modifications to avoid triggers for the condition are also recommended.
Corticosteroid creams are sometimes prescribed to decrease the inflammatory reaction in the skin. These may be mild-, medium-, or high-potency corticosteroid creams depending upon the severity of the symptoms. If itching is severe, oral antihistamines may be prescribed. To control itching, the sedative type antihistamine drugs (for example, diphenhydramine [Benadryl], hydroxyzine [Atarax, Vistaril], and cyproheptadine) appear to be most effective.
Learn more about: Benadryl | Vistaril | cyproheptadine
In some cases, a short course of oral corticosteroids (such as prednisone) is prescribed to control an acute outbreak of eczema, although their long-term use is discouraged in the treatment of this non life-threatening condition because of unpleasant and potentially harmful side effects. The oral immunosuppressant drug cyclosporine has also been used to treat some cases of eczema. Ultraviolet light therapy (phototherapy) is another treatment option for some people with eczema.
Finally, two topical (cream) medications have been approved by the U.S. FDA for the treatment of eczema: tacrolimus (Protopic) and pimecrolimus (Elidel). These drugs belong to a class of immune suppressant drugs known as calcineurin inhibitors and are indicated only in patients over 2 years of age. In January 2006, the FDA issued a black box warning stating the long-term safety of calcineurin inhibitors has not been established. Although a causal relationship has not been established, rare cases of malignancy have been reported with their use. It is recommended that these drugs only be used as second-line therapy for cases that are unresponsive to other forms of treatment and that their use be limited to the minimum time periods needed to control symptoms. Use of these drugs should also be limited in people who have compromised immune systems.
While there is no cure for eczema, you can take steps to manage your symptoms and lessen the severity of outbreaks. Such measures include
Atrial fibrillation (AF) is the most common, abnormal rhythm of the heart.
The heart contracts (beats) and pumps blood with a regular rhythm, for example, at a rate of 60 beats per minute there is a beat every second. The heart may beat faster or slower with a shorter or longer interval between beats, but at any one rate the interval between beats is constant. This regular rhythm occurs as a result of regular electrical discharges (currents) that travel through the heart and cause the muscle of the heart to contract. In atrial fibrillation, the electrical discharges are irregular and rapid and, as a result, the heart beats irregularly and, usually, rapidly.
Atrial fibrillation is common; half a million new cases are diagnosed yearly in the U.S., and billions of dollars are spent annually on its diagnosis and treatment.
Normal function of the heart
The heart has four chambers. The upper two chambers are the atria, and the lower two chambers are the ventricles. Blood returning to the heart from the body in the superior and inferior vena cava contains low levels of oxygen and high levels of carbon dioxide. This blood flows into the right atrium and then into the adjacent right ventricle. After the ventricle fills, contraction of the right atrium pumps additional blood into the right ventricle. The right ventricle then contracts and pumps the blood to the lungs where the blood takes up oxygen and gives off carbon dioxide. The blood then flows from the lungs to the left atrium and into the adjacent left ventricle. Contraction of the left atrium pumps additional blood into the left ventricle. The left ventricle then contracts and pumps the blood to the rest of the body. The heartbeat (pulse) that we feel is caused by the contraction of the ventricles.
The ventricles must deliver enough blood to the body for the body to function normally. The amount of blood that is pumped depends on several factors. The most important factor is the rate of contraction of the heart (the heart rate). As the heart rate increases, more blood is pumped. In addition, the heart pumps more blood with each beat when the atria contract and fill the ventricles with additional blood just before the ventricles contract.
With each beat of the heart, an electrical discharge (current) passes through the electrical system of the heart. The electrical discharge causes the muscle of the atria and ventricles to contract and pump blood. The electrical system of the heart consists of the SA node (sino-atrial node), the AV node (atrio-ventricular node) and special tissues in the atria and the ventricles that conduct the current.
The SA node is the heart's electrical pacemaker. It is a small patch of cells located in the wall of the right atrium; the frequency with which the SA node discharges determines the rate at which the heart beats. The electrical current passes from the SA node, through the special tissues of the atria and into the AV node. The AV node serves as an electrical relay station between the atria and the ventricles. Electrical signals from the atria must pass through the AV node to reach the ventricles.
The electrical discharges from the SA node cause the atria to contract and pump blood into the ventricles. The same discharges then pass through the AV node to reach the ventricles, traveling through the special tissues of the ventricles and causing the ventricles to contract. In a normal heart, the rate of atrial contraction is the same as the rate of ventricular contraction.
At rest, the frequency of the electrical discharges originating from the SA node is low, and the heart beats at the lower range of normal (60-80 beats/minute). During exercise or excitement, the frequency of discharges from the SA node increases, increasing the rate at which the heart beats.
Function of the heart during atrial fibrillation
During atrial fibrillation, electrical discharges are not generated solely by the SA node. Instead, electrical discharges come from other parts of the atria. These abnormal discharges are rapid and irregular and may exceed 350 discharges per minute. The rapid and irregular discharges cause ineffective contractions of the atria. In fact, the atria quiver rather than beat as a unit. This reduces the ability of the atria to pump blood into the ventricles.
The rapid and irregular electrical discharges from the atria then pass through the AV node and into the ventricles, causing the ventricles to contract irregularly and (usually) rapidly. The contractions of the ventricles may average 150/minute, much slower than the rate in the atria. (The ventricles are unable to contract at 350/minute.) Even at an average rate of 150/minute, the ventricles may not have enough time to fill maximally with blood before the next contraction, particularly without the normal contraction of the atria. Thus, atrial fibrillation decreases the amount of blood pumped by the ventricles because of their rapid rate of contraction and the absence of normal atrial contractions.
Heart rate during atrial fibrillation
In a heart that is beating normally, the rate of ventricular contraction is the same as the rate of atrial contraction. In atrial fibrillation, however, the rate of ventricular contraction is less than the rate of atrial contraction. The rate of ventricular contraction in atrial fibrillation is determined by the speed of transmission of the atrial electrical discharges through the AV node. In people with a normal AV node, the rate of ventricular contraction in untreated atrial fibrillation usually ranges from 80 to 180 beats/minute; the higher the transmission, the higher the heart rate.
Some older people have slow transmission through the AV node due to disease within the AV node. When these people develop atrial fibrillation, their heart rates remain normal or slower than normal. As disease in the AV node advances, these people can even develop an excessively slow heart rate and require a permanent pacemaker to increase the rate of ventricular contractions.
Many patients with atrial fibrillation have no symptoms and are unaware of the abnormal heart rhythm. The most common symptom of atrial fibrillation is palpitations, an uncomfortable awareness of the rapid and irregular heartbeat. Other symptoms of atrial fibrillation are caused by the diminished delivery of blood to the body. These symptoms include
If the heart is unable to pump an adequate amount of blood to the body, as in some people with atrial fibrillation, the body begins to compensate by retaining fluid. This can lead to a condition called heart failure. Heart failure results in the accumulation of fluid in the lower legs (edema) and the lungs (pulmonary edema). Pulmonary edema makes breathing more difficult and reduces the ability of the lung to add oxygen to and remove carbon dioxide from the blood. The levels of oxygen in the blood can drop, and the levels of carbon dioxide in the blood can rise, a complication called respiratory failure. This is a life-threatening complication.
Quivering of the atria in atrial fibrillation cause blood inside the atria to stagnate. Stagnant blood tends to form blood clots along the walls of the atria. Sometimes, these blood clots dislodge, pass through the ventricles, and lodge in the brain, lungs, and other parts of the body. This process is called embolization. One common complication of atrial fibrillation is a blood clot that travels to the brain and causes the sudden onset of one-sided paralysis of the extremities and/or the facial muscles (an embolic stroke). A blood clot that travels to the lungs can cause injury to the lung tissues (pulmonary infarction), and symptoms of chest pain and shortness of breath. When blood clots travel to the body's extremities, cold hands, feet, or legs may occur suddenly because of the lack of blood.
There are many risk factors for developing atrial fibrillation. These risk factors are:
About 1 in 10,000 otherwise healthy, young adults have atrial fibrillation without any apparent cause or underlying heart disease. Atrial fibrillation in these individuals usually is intermittent, but can become chronic in 25%. This condition is referred to as lone atrial fibrillation. Stress, alcohol, tobacco, or use of stimulants may play a role in causing lone atrial fibrillation.
Atrial fibrillation can be chronic and sustained, or brief and intermittent (paroxysmal). Paroxysmal atrial fibrillation refers to intermittent episodes of atrial fibrillation lasting, for example, minutes to hours. The heart rate reverts to normal between episodes. In chronic, sustained atrial fibrillation, the atria fibrillate all of the time. Chronic, sustained atrial fibrillation is not difficult to diagnose. Doctors can hear the rapid and irregular heartbeats using a stethoscope. Abnormal heartbeats also can be felt by taking a patient's pulse.
An electrocardiogram (EKG) is a brief recording of the heart's electrical discharges. The irregular EKG tracings of atrial fibrillation are easy to recognize provided atrial fibrillation occurs during the EKG.
If episodes of atrial fibrillation occur intermittently, a standard EKG performed at the time of a visit to the doctor's office may not show atrial fibrillation. Therefore, a Holter monitor, a continuous recording of the heart's rhythm for 24 hours, often is used to diagnose intermittent episodes of atrial fibrillation.
Patient-activated event recorder
If the episodes of atrial fibrillation are infrequent, a 24-hour Holter recording may not capture these sporadic episodes. In this situation, the patient can wear a patient-activated event recorder for 1 to 4 weeks. The patient presses a button to start the recording when he or she senses the onset of irregular heartbeats or symptoms possibly possible caused by atrial fibrillation. The doctor then analyzes the recordings at a later date.
Echocardiography uses ultrasound waves to produce images of the heart's chambers and valves and the lining around the heart (pericardium). Conditions that may accompany atrial fibrillation such as mitral valve prolapse, rheumatic valve diseases, and pericarditis (inflammation of the "sack" surrounding the heart) can be detected with echocardiography. Echocardiography also is useful in measuring the size of the atrial chambers. Atrial size is an important factor in determining how a patient responds to treatment for atrial fibrillation. For instance, it is more difficult to achieve and maintain a normal heart rhythm in patients with enlarged atria.
Transesophageal echocardiography (TEE)
Transesophageal echocardiography (TEE) is a special echocardiographic technique that involves taking pictures of the atria using sound waves. A special probe that generates sound waves is placed in the esophagus (the food pipe connecting the mouth to the stomach). The probe is located at the end of a long flexible tube that is inserted through the mouth into the esophagus. This technique brings the probe very close to the heart (which lies just in front of the esophagus). Sound waves generated by the probe are bounced off of the structures within the heart, and the reflected sound waves are used to form a picture of the heart. TEE is very accurate for detecting blood clots in the atria as well as for measuring the size of the atria.
As previously discussed, blood may clot in the atria during atrial fibrillation, and pieces of the clot may dislodge and travel to the brain, causing a stroke. Doctors are especially concerned about blood clots dislodging during or after cardioversion (the conversion of atrial fibrillation back into a normal heart rhythm with either drugs or electrical shocks). Moreover, doctors believe that resumption of atrial contractions after successful cardioversion increases the likelihood that pieces of clot will dislodge. For these reasons, anticoagulation (thinning) of blood usually is done prior to cardioversion. This prevents new clot from forming while the old clot dissolves or solidifies so that pieces cannot break off. If no clots are detected in the atria by TEE, the risk of stoke after cardioversion is believed to be lower. Thus, some doctors use TEE to determine the risk of stroke following cardioversion. Studies are underway to determine whether patients with a normal TEE (no blood clots) need to have their blood thinned prior to cardioversion.
High blood pressure and signs of heart failure can be ascertained (determined) during a physical examination of the patient. Blood tests are performed to detect abnormalities in blood oxygen and carbon dioxide levels, electrolytes, and thyroid hormone levels. Chest X-rays reveal enlargement of the heart, heart failure, and other diseases of the lung. Exercise treadmill testing (a continuous recording of the EKG during exercise) is a useful screening study for detecting severe coronary artery disease.
The treatment of atrial fibrillation is multi-faceted and involves
An important first step in the treatment of atrial fibrillation is to uncover and correct conditions (such as hyperthyroidism or use of stimulant drugs) that can cause atrial fibrillation. These steps include:
Having excluded or corrected the factors that cause atrial fibrillation, the next step when the ventricles are beating too rapidly usually is to slow the rate at which the ventricles beat.
Available medications. Patients with atrial fibrillation and healthy AV nodes usually have ventricles that beat rapidly. Medications are necessary to slow down the rapid heart rate. Medications to slow the heart rate in atrial fibrillation include:
Learn more about: Inderal | Lopressor | Brevibloc | Calan | Cardizem
These medications slow the heart rate by retarding conduction of the electrical discharges through the AV node. These medications, however, do not usually convert atrial fibrillation back into a normal rhythm. Other drugs or treatments are necessary to achieve a normal heart rhythm.
Benefits of controlling the rate. In patients with rapid ventricle contractions as a result of atrial fibrillation, slowing the rate of ventricular contractions improves the heart's efficiency in delivering blood (by allowing more time between contractions for the ventricles to fill with blood) and relieves the symptoms of inadequate flow of blood - dizziness, weakness, and shortness of breath.
With chronic, sustained atrial fibrillation, doctors may decide to leave some patients in atrial fibrillation provided that their heart rates are under control, the output of blood from the ventricles is adequate, and their blood is adequately thinned to prevent strokes. This form of treatment is called rate control therapy (see below).
Limitations of medications for controlling the heart rate. In patients with diseased AV nodes, ventricular contractions may be slower than patients who have normal AV nodes. Moreover, some elderly patients with atrial fibrillation are extremely sensitive to medications that slow the rate of ventricular contractions, usually because of a diseased AV node. In these patients, the heart rate can become dangerously slow with small doses of medications to slow the heart. This condition is referred to as tachycardia-bradycardia syndrome, or "sick sinus syndrome." Patients with tachycardia-bradycardia syndrome need medications to control the fast heart rate and a pacemaker to provide a minimum safe heart rate.
Medications used in slowing atrial fibrillation generally cannot convert atrial fibrillation to a normal rhythm. Therefore these patients are at risk for the formation of blood clots in the heart and strokes and will need prolonged blood thinning with anticoagulants like warfarin (Coumadin).
Atrial fibrillation is one of the most important causes of stroke in the U.S. Warfarin (Coumadin) is a blood thinner that prevents the formation of blood clots. Studies in patients with chronic sustained atrial fibrillation and sporadic (paroxysmal) atrial fibrillation have shown that warfarin reduces strokes.
Aspirin is an anti-platelet agent. Platelets are elements in the blood that are necessary for blood clots to form. Aspirin can be considered a milder blood thinner than warfarin, but it is not as reliable as warfarin in preventing strokes in patients with atrial fibrillation. Some doctors prescribe aspirin to patients when the risk of bleeding from warfarin is believed to be too high and to patients who refuse to take warfarin. Young patients with lone atrial fibrillation who are not at an increased risk for stroke sometimes are given aspirin rather than warfarin.
Side effects of warfarin. There are some patients who are at increased risk for side effects from warfarin. Specifically:
Because of these serious side effects, patients using warfarin must be closely monitored with clotting tests such as the INR. The INR is a blood test that measures the degree of blood thinning. (The higher the value for the INR, the thinner the blood.) In preventing strokes in patients with atrial fibrillation, the dose of warfarin is adjusted to achieve a "therapeutic range" of INR. INR values higher than the therapeutic range are associated with an increased risk for bleeding, while values below the therapeutic range are associated with a diminished effectiveness in preventing stroke. Patients who are unreliable or unwilling to be monitored with regular measurements of INR may be considered for aspirin treatment rather than warfarin.
The beneficial effect of warfarin in preventing strokes needs to be balanced against the risk of excessive bleeding if the blood becomes too thin.
Candidates for warfarin. Doctors recommend warfarin to most elderly patients 65 years of age or older with paroxysmal (recurrent episodes) or chronic sustained atrial fibrillation. On balance, elderly patients with atrial fibrillation are more likely to benefit from warfarin because they are at a particularly high risk for stroke.
Patients younger than 65 with atrial fibrillation, especially those with prior embolic strokes, significant diseases of the heart, diabetes mellitus, high blood pressure, heart failure, coronary artery disease of the heart, or abnormally enlarged atrial chambers also are candidates for warfarin.
Patients who are not candidates for warfarin. Patients who are not candidates for warfarin include:
Converting atrial fibrillation to a normal rhythm can be accomplished with medications (chemical cardioversion) or by electrical shocks (electrical cardioversion). Doctors usually recommend that all patients with chronic sustained atrial fibrillation undergo at least one attempt at cardioversion, chemical or electrical. Successful cardioversion can alleviate symptoms, improve exercise tolerance, improve quality of life, and lower the risk of strokes. Doctors usually try medical cardioversion first, and, if medications fail, then try electrical cardioversion.
Patients who are more likely to attain and maintain a normal heart rhythm with either chemical or electrical cardioversion include:
Cardioversion with medications. Before prescribing medications for cardioversion, the doctor usually controls the rate of ventricular contractions and thins the blood, usually with warfarin.
1) Available Medications. Medications used in cardioversion usually work by blocking the channels in the walls of cells through which ions travel (sodium channels, potassium channels, beta adrenergic channels, and calcium channels). Some examples of these medications include:
- quinidine (Quinaglute)
- procainamide (Procan SR)
- disopyramide (Norpace)
- flecainide (Tambocor)
- sotalol (Betapace)
- flecainide (Tambocor)
- amiodarone (Cordarone)
Learn more about: Procan SR | Norpace | Tambocor | Betapace | Cordarone
These medications are capable of converting atrial fibrillation to normal rhythm in about 50% of patients. They often are used long-term to maintain a normal rhythm and prevent recurrences of atrial fibrillation.
2) Disadvantages of using medications. Medications used for converting atrial fibrillation carry a small risk of causing other abnormal heart rhythms--they are said to be pro-arrhythmic--especially in patients with diseases of the heart muscle or coronary arteries. These abnormal heart rhythms can be more life-threatening than atrial fibrillation. Therefore, treatment with these medications often is initiated in the hospital while the patient's rhythm is continuously monitored for 24-72 hours.
These medications may not be effective in the longer-term. Many patients eventually develop a recurrence of atrial fibrillation despite the medications.
Medications used in treating atrial fibrillation often have important side effects. Many patients discontinue them because they cannot tolerate these side effects. For example, amiodarone is commonly used in treating atrial fibrillation because it is less pro-arrhythmic and has been shown to maintain a normal rhythm in up to 75% of patients. However, amiodarone frequently causes side effects and drug interactions. About 7 out of every 10 patients taking amiodarone experience some type of side effect, and between 1 in 5 and 1 in 20 experience side effects that are severe enough that the amiodarone must be stopped. Amiodarone can interact with other medications such as tricyclic antidepressants, for example, amitriptyline (Elavil, Endep) or phenothiazine antipsychotics, for example, chlorpromazine (Thorazine) and cause abnormal heart rhythms. Amiodarone interacts with warfarin and increases the risk of bleeding. This interaction with warfarin can occur as early as 4-6 days after the start of both drugs or can be delayed by a few weeks. Thus, doctors prescribing both warfarin and amiodarone will adjust the dose of warfarin to avoid excessive blood thinning. Amiodarone also can cause thyroid disturbances in the fetus when administered orally to the mother during pregnancy. Amiodarone also may affect thyroid function in adults. The most severe side effect of amiodarone is lung toxicity that potentially can be fatal. Because of this lung toxicity, patients should report any symptoms of cough, fever, or painful breathing to their doctors.
Electrical cardioversion. Electrical cardioversion is a procedure used by doctors to convert an abnormal heart rhythm (such as atrial fibrillation) to a normal rhythm (sinus rhythm). Electrical cardioversion requires the administration of an electrical shock over the chest. This electrical shock stops the abnormal electrical activity of the heart for a brief moment and allows the normal heart rhythm to take over. Although electrical cardioversion can be used to treat almost any abnormal fast heartbeat (such as atrial flutter and ventricular tachycardia), it is used most frequently to convert atrial fibrillation to a normal rhythm.
Warfarin usually is given for 3 to 4 weeks prior to cardioversion to minimize the risk of stroke that can occur during or shortly after cardioversion. Warfarin is continued for four to six weeks after successful cardioversion. For some patients requiring urgent electrical cardioversion, warfarin may not work fast enough to thin the blood. Therefore, these patients may be given heparin prior to electrical cardioversion. Heparin is a faster-acting blood thinner than warfarin, but it must be administered as a continuous intravenous infusion or as injections under the skin. After successful cardioversion, these patients can be switched from heparin to warfarin.
Learn more about: heparin
1) Method of cardioversion. Electrical cardioversions (urgent and elective) usually are performed in a hospital. For elective (non-urgent) electrical cardioversion, patients usually arrive at the hospital without eating in the morning. Necessary medications can be taken with small sips of water. Patients are given supplemental oxygen via nasal catheters, and an intravenous infusion of fluids is started. Electrodes (pads) are placed on the skin over the chest to continuously monitor the heart rhythm. Paddles then are placed over the chest and the upper back. Patients are sedated (anesthetized) intravenously with medications. This is followed by a strong electric shock through the paddles. The shock converts the atrial fibrillation to a normal rhythm. After cardioversion, patients are observed for several hours or overnight to make sure that their normal heart rhythm is stable.
2) Effectiveness of electrical cardioversion. Electrical cardioversion is more effective than medications alone in terminating atrial fibrillation and restoring a normal heart rhythm. Electrical cardioversion successfully restores a normal heart rhythm in over 95% of patients.
3) Limitations of electrical cardioversion. While electrical cardioversion is effective in converting atrial fibrillation to a normal heart rhythm, the normal rhythm may not continue for long. Approximately 75% of patients successfully treated with electrical cardioversion experience a recurrence of atrial fibrillation within 12-24 months. Older patients with enlarged atria and ventricles who have had atrial fibrillation for a long time are especially prone to recurrences. Thus, most patients who undergo successful cardioversion are placed on oral medications to prevent recurrences of atrial fibrillation.
4) Risks of electrical cardioversion. The risks of electrical cardioversion include stroke, heart attack, burns of the skin, and in rare instances, death.
5) Candidates for electrical cardioversion. Doctors usually recommend that all patients with chronic, sustained atrial fibrillation undergo at least one attempt at cardioversion. Cardioversion usually is attempted with medications first. If medications fail, electrical cardioversion can be considered. Sometimes a doctor may choose to use electrical cardioversion first if atrial fibrillation is of short duration (onset within 48 hours) and the transesophageal echocardiography shows no blood clots in the atria.
Electrical cardioversion is performed urgently (on an emergency basis) on patients with severe and potentially life-threatening symptoms caused by atrial fibrillation. For example, some patients with rapid atrial fibrillation can develop chest pain, shortness of breath, and dizziness or fainting. (Chest pain in these patients is due to an insufficient supply of blood to the heart muscles. Shortness of breath indicates ineffective pumping of blood by the ventricles. Fainting or dizziness usually is due to dangerously low blood pressure.)
Rate control therapy. Recent studies have shown that an acceptable alternative to cardioversion (chemical or electrical) is rate-control therapy. In rate-control therapy, the doctor will leave the patients in atrial fibrillation provided their rate of ventricular contractions is under good control, the output of blood from the heart is adequate, and their blood is adequately thinned by warfarin to prevent strokes. Heart rate in these patients can be controlled using medications such as beta-blockers, calcium channel blockers, or digoxin or AV node ablation with pacemaker implantation. Rate-control therapy is used to simplify therapy and avoid the side effects of anti-arrhythmic medications (medications used to treat and prevent atrial fibrillation).
Over long periods of observation, patients treated with rate-control therapy have similar survival and quality of life as compared to patients who undergo repeated electrical or chemical cardioversions.
Suitable candidates for rate-control therapy include:
After successful cardioversion many patients (up to 75%) may experience recurrence of atrial fibrillation within 12 months. Therefore, many patients will need long-term treatment with medications to prevent a recurrence of atrial fibrillation; however, medication(s) are effective only 50%-75% of the time in preventing recurrence. Moreover, many patients cannot tolerate the side effects of long-term medication. For these reasons, several procedures have been developed to treat and prevent recurrence of atrial fibrillation; they include:
Ablation of the AV node with implantation of a pacemaker. Ablation of the AV node is a procedure that destroys the AV node so that the atrial electrical discharges cannot pass through the AV node to activate the ventricles. The procedure usually is performed in a cardiac catheterization unit or an electrophysiology unit of a hospital.
1) Procedure. For ablation of the AV node, patients are given a local anesthetic to minimize pain and are mildly sedated with intravenous medications. Using x-ray guidance, a wire (catheter) is inserted through a vein in the groin to reach the heart. Electrical recordings from inside the heart help to locate the AV node. The AV node is destroyed (ablated) using heat delivered by the catheter. After successful ablation of the AV node, electrical discharges from the atria can no longer reach the ventricles. Destruction of the AV node (whether by catheter ablation or by disease that occurs with age) can lead to an excessively slow rate of ventricular contractions (slow heart rate). Therefore, a pacemaker is implanted in order to provide the heart with a minimum safe heart rate.
2) Benefits of ablation of the AV node. The benefits of ablation of the AV node and implantation of a pacemaker include:
- resumption of a regular heart rate (even though a pacemaker may be determining the heart rate)
- relief from palpitations, fainting, dizziness, and shortness of breath
- ability to stop medications and avoid their potentially serious side effects
3) Risks of ablation of the AV node. Potential complications of ablation of the AV node and permanent implantation of a pacemaker include bleeding, infection, heart attack, stroke, introduction of air into the space between the lung and chest wall, and death. Still, this technique has helped many patients with severe symptoms to live normally.
4) Candidates for ablation of the AV node. Candidates for ablation of the AV node are patients with atrial fibrillation who respond poorly to both chemical and electrical cardioversion. These patients experience repeated relapses of atrial fibrillation, often with rapid rates of ventricular contractions despite medications. Ablation also may be an option for patients who develop serious side effects from the medications that are used for treating and preventing atrial fibrillation.
5) Limitations of ablation of the AV node. Ablation of the AV node only controls the rate with which the ventricles beat. It does not convert atrial fibrillation to normal rhythm. Therefore, blood clots still can form in the atria and patients are still at risk of strokes. Thus, there is a need for long-term anticoagulation in addition to the permanent pacemaker.
Pacemakers. Permanent pacemakers are battery-operated devices that generate electrical discharges that cause the heart to beat more rapidly when the heart is beating too slowly. Recent studies suggest that some patients with recurrent paroxysmal atrial fibrillation can benefit from the implantation of a permanent pacemaker. Although the reasons for this benefit are unknown, regular electrical pulses from the pacemakers may prevent the recurrence of atrial fibrillation. Furthermore, newer pacemakers that can stimulate two different sites within the atria (dual site atrial pacing) may be even more effective than standard pacemakers in preventing atrial fibrillation. Nevertheless, permanent pacemaker implantation cannot be considered as standard non-medication treatment for atrial fibrillation.
Implantable atrial defibrillators. Implantable atrial defibrillators can detect and convert atrial fibrillation back to a normal rhythm by using high-energy shocks. By detecting atrial fibrillation and terminating it quickly, doctors hope that these devices will prevent recurrences of atrial fibrillation over the long term.
Atrial defibrillators are surgically implanted within the chest under local anesthesia. These devices deliver high-energy shocks to the heart that are somewhat painful. Atrial defibrillators are not useful in patients with chronic sustained atrial fibrillation and are suitable only for patients with infrequent episodic attacks of atrial fibrillation.
Maze procedure. Many doctors believe that the atria cannot fibrillate if they are sectioned into small pieces so that the conduction of the electrical current through the atria is interrupted. During the Maze procedure, numerous incisions are made in the atria to control the irregular heartbeat and restore a regular rhythm to the heart.
1) Procedure. The Maze procedure is most commonly performed via open-heart surgery. Some electrophysiologists (doctors specially trained to treat abnormalities of rhythm) are now attempting to perform the Maze procedure using catheters inside the heart that are passed through a vein in the groin without open-heart surgery. Unfortunately, the success rate using the catheter is below 50% and complications (such as strokes) may occur.
2) Effectiveness of the Maze procedure. The Maze procedure done surgically (using open heart surgery) has been reported to correct atrial fibrillation in 90-99% of patients. Only 15-20% of the patients need a pacemaker after surgery, and there is only a 30% chance of requiring long-term medications to maintain a normal rhythm.
3) Risks of the Maze procedure. The surgical maze procedure involves open-heart surgery and the pumping of blood by an external bypass pump while the surgery is performed, much like patients undergoing cardiac bypass surgery. The complications are not insignificant and include stroke, bleeding, infection, and death. Therefore, doctors usually do not recommend a surgical Maze procedure for the treatment of atrial fibrillation unless the patient is undergoing open-heart surgery for another condition (such as for coronary artery bypass or replacement or repair of a diseased heart valve).
Pulmonary vein isolation
The four pulmonary veins are blood vessels that carry oxygen-rich blood from the lungs to the left atrium. There is a narrow band of muscle cells that surrounds the openings of the pulmonary veins where they enter the left atrium. This band of muscle cells may begin to actively discharge electrically, and this discharge may initiate atrial fibrillation. During pulmonary vein isolation (PVI), the band of muscle cells is destroyed by energy applied through a catheter. This effectively blocks the electrical discharges from crossing over from the band to the left atrium and hence prevents atrial fibrillation.
Procedure. Before PVI, the doctor performs a history and physical examination, an EKG, a 24-hour Holter monitor, and a trans-esophageal echocardiogram to exclude blood clots in the atria, and, sometimes, a CAT scan of the chest. The doctor also may ask the patient to stop certain medications, particularly blood thinners such as aspirin, clopidogrel (Plavix), or warfarin, several days before the procedure. The doctor may check a blood prothrombin time and INR level to make sure that blood clotting is adequate for the procedure.
Learn more about: Plavix
PVI is performed under deep conscious sedation (but not general anesthesia) in a cardiac electro-physiology laboratory and takes three to six hours. Several catheters are inserted through large veins (in the neck, arm or groin) and fed into the left atrium under x-ray (fluoroscopy) guidance. One of the catheters is equipped with an ultrasound transducer that allows the doctor to view the structures inside the heart during the procedure. The junction of the pulmonary veins with the left atrium is identified, and energy is then applied through another catheter to this area. This results in the destruction of the band of muscle cells and their replacement by a scar. This process is repeated at the opening of each of the four pulmonary veins into the left atrium.
Course post-pulmonary vein isolation. After PVI, patients remain in the hospital telemetry unit for several days so that the heart's rhythm can be monitored.
Many patients will experience atrial fibrillation and palpitations (irregular heart beat) while in the hospital and during the first two or three months following PVI. Therefore, they are given medications such as amiodarone to prevent episodes of atrial fibrillation and anticoagulation with medications such as warfarin to prevent strokes. The palpitations and episodes of atrial fibrillation gradually decrease. By three months after the procedure, the majority of patients will have a normal rhythm, and the doctor may stop warfarin and amiodarone.
Patients usually will have an EKG and a CAT scan of the chest three months after PVI. The CAT scan is done to make sure that there is no narrowing of the pulmonary veins (pulmonary vein stenosis) due to the scarring.
Effectiveness of pulmonary vein isolation. PVI in the U.S. is a new procedure. Most cardiologists in the U.S. have limited experience with PVI. When performed by experienced doctors, PVI can be expected to prevent atrial fibrillation in 70% to 80% of patients during the first year. Some patients may need additional PVI procedures to prevent further atrial fibrillation episodes. Because this procedure is new, it is difficult to know whether successfully-treated patients will continue in a normal rhythm for a prolonged period of time.
Risks of pulmonary vein isolation. When performed by doctors experienced in PVI, the procedure is safe. The risks of pulmonary vein isolation include cardiac tamponade (bleeding into the pericardium, the sac surrounding the heart), narrowing of the openings of the pulmonary veins, injury to the phrenic nerve that controls the function of the diaphragm, injury to peripheral blood vessels, and, in rare cases, death.
In the early years of PVI, doctors were trying to destroy the tissues inside the pulmonary veins. This led to narrowing (due to scarring) of the pulmonary veins which, in turn, led to pulmonary hypertension, a condition in which the blood pressure in the pulmonary veins and arteries increases. Pulmonary hypertension is a serious condition that can lead to heart failure and even death. Doctors no longer try to destroy tissue inside the pulmonary veins. Instead, they try to destroy the tissues only at the junction of the pulmonary veins and the atria. The current technique is not only safer but is more effective and simpler.
Candidates for pulmonary vein isolation. Generally, good candidates for PVI include: