abdominal diseases

Toothache

2012-03-17T04:35:00.001-07:00

What is a toothache?

"Toothache" usually refers to pain around the teeth or jaws primarily as a result of a dental condition. In most instances, toothaches are caused by tooth problems, such as a dental cavity, a cracked tooth, an exposed tooth root, or gum disease. However, disorders of the jaw joint (temporo-mandibular joint) can also cause pain that is referred to as "toothache." The severity of a toothache can range from chronic and mild to sharp and excruciating. The pain may be aggravated by chewing or by cold or heat. A thorough oral examination, which includes dental X-rays, can help determine whether the toothache is coming from a tooth or jaw problem and the cause.
Sometimes, a toothache may be caused by a problem not originating from a tooth or the jaw. Pain around the teeth and the jaws can be symptoms of diseases of the heart (such as angina or heart attack), ears (such as inner or external ear infections), and sinuses (air passages of the cheekbones). For example, the pain of angina (inadequate supply of oxygenated blood to the heart muscle because of narrowing of the arteries to the heart) is usually located in the chest or the arm. However, in some patients with angina, a toothache or jaw pain is the only symptom of their heart problem. Infections and diseases of the ears and sinuses can also cause pain around the teeth and jaws. Therefore, evaluations by both dentists and doctors are sometimes necessary to diagnose medical illnesses causing "toothache."

What are dental causes of toothaches?

Common dental causes of toothaches include dental cavities, dental abscess, gum disease, irritation of the tooth root, cracked tooth syndrome, temporomandibular joint (TMJ) disorders, impaction, and eruption.
Dental cavities & dental abscess
The most common cause of a toothache is a dental cavity. Dental cavities (caries) are holes in the two outer layers of a tooth called the enamel and the dentin. The enamel is the outermost white hard surface and the dentin is the yellow layer just beneath the enamel. Both layers serve to protect the inner living tooth tissue called the pulp, where blood vessels and nerves reside. Certain bacteria in the mouth convert simple sugars into acid. The acid softens and (along with saliva) dissolves the enamel and dentin, creating cavities. Small, shallow cavities may not cause pain and may be unnoticed by the patient. The larger deeper cavities can be painful and collect food debris. The inner living pulp of the affected tooth can become irritated by bacterial toxins or by foods and liquids that are cold, hot, sour, or sweet, thereby causing toothaches. Severe injury to the pulp can lead to the death of pulp tissue, resulting in tooth infection (dental abscess). A small swelling or "gum blister" may be present near the affected tooth as well. Toothaches from these larger cavities are the most common reason for visits to dentists.
Treatment of a small and shallow cavity usually involves a dental filling. Treatment of a larger cavity involves an onlay or crown. Treatment for a cavity that has penetrated and injured the pulp or for an infected tooth is either a root canal procedure or extraction of the affected tooth. The root canal procedure involves removing the dying pulp tissue (thus avoiding or removing tooth infection) and replacing it with an inert filling material. The procedure is used in an attempt to save the dying tooth from extraction. Once a root canal procedure is done, the tooth is more prone to fracture and will oftentimes require a crown to protect it.
Gum disease
The second most common cause of toothache is gum disease (periodontal disease). Gum disease refers to inflammation of the soft tissue (gingiva) and abnormal loss of bone that surrounds and holds the teeth in place. Gum disease is caused by toxins secreted by certain bacteria in "plaque" that accumulate over time along and under the gum line. This plaque is a mixture of food, saliva, and bacteria. An early symptom of gum disease is gum bleeding without pain. Pain is a symptom of more advanced gum disease as the loss of bone around the teeth leads to the formation of deep gum pockets. Bacteria in these pockets cause gum infection, swelling, pain, and further bone destruction. Advanced gum disease can cause loss of otherwise healthy teeth. Gum disease is complicated by such factors as poor oral hygiene, family history of gum disease, smoking, and family history of diabetes.
Treatment of gum disease always involves oral hygiene and removal of bacterial plaque and tartar (hardened plaque). Moderate to advanced gum disease usually requires a thorough cleaning of the teeth and teeth roots called "scaling and root planing" and "subgingival curettage." Scaling and root planing is the removal of plaque and tartar from exposed teeth roots while subgingival curettage refers to the removal of the surface of the inflamed layer of gum tissue. Both of these procedures are usually performed under local anesthesia and may be accompanied by the use of oral antibiotics to overcome gum infection or abscess. Follow-up treatment, if necessary, may include various types of gum operations. In advanced gum disease with significant bone destruction and loosening of teeth, teeth splinting or teeth extractions may be necessary.
Tooth root sensitivities
Toothache can also be caused by exposed tooth roots. Typically, the roots are the lower two-thirds of the teeth that are normally buried in bone. The bacterial toxins dissolve the bone around the roots and cause the gum and the bone to recede, exposing the roots. The condition of exposed roots is called "recession." The exposed roots can become extremely sensitive to cold, hot, and sour foods because they are no longer protected by healthy gum and bone.
Early stages of root exposure can be treated with topical fluoride gels applied by the dentist or with special toothpastes (such as Sensodyne or Denquel) which contain fluorides and other minerals. These minerals are absorbed by the surface layer of the roots to make the roots stronger and less sensitive to the oral environment. Dentists may also apply "bonding agents" to the exposed roots to seal the sensitive areas. If the root exposure causes injury and death of the inner living pulp tissue of the tooth, then a root canal procedure or tooth extraction may be necessary.
Cracked tooth syndrome
"Cracked tooth syndrome" refers to a toothache caused by a broken tooth (tooth fracture) without associated cavity or advanced gum disease. Biting on the area of tooth fracture can cause severe sharp pains. These fractures are usually due to chewing or biting hard objects such as hard candies, pencils, nuts, etc. Your dentist can usually detect the fracture by painting a special dye on the cracked tooth or shining a special light on the tooth. Treatment usually involves protecting the tooth with a full-coverage crown made of gold and/or porcelain. However, if placing a crown does not relieve pain symptoms, a root canal procedure may be necessary.
Temporomandibular joint (TMJ) disorders
Disorders of the temporomandibular joint(s) can cause pain which usually occurs in or around the ears or lower jaw. The TMJ hinges the lower jaw (mandible) to the skull and is responsible for the ability to chew or talk. TMJ disorders can be caused by different types of problems such as injury (such as a blow to the face), arthritis, or jaw muscle fatigue from habitually clenching or grinding teeth. Habitual clenching or grinding of teeth, a condition called "bruxism," can cause pain in the joints, jaw muscles, and the teeth involved. Bruxism is often due to life "stress," family history of bruxism, and poor bite alignment. Sometimes, muscles around the TMJ used for chewing can go into spasm, causing head and neck pain and difficulty opening the mouth normally. These muscle spasms are aggravated by chewing or by stress, which cause the patients to clench their teeth and further tighten these muscles. Temporary TMJ pain can also result from recent dental work or by the trauma of extracting impacted wisdom teeth.
Treatment of temporo-mandibular joint pain usually involves oral anti-inflammatory over-the counter (OTC) drugs like ibuprofen (Motrin or Advil) or naproxen (Aleve). Other measures include warm moist compresses to relax the joint areas, stress reduction, and/or eating soft foods that do not require much chewing. If bruxism is diagnosed by a dentist, a bite appliance (night guard) may be recommended that is worn during the night to protect the teeth. However, this bite appliance is used mainly to protect the teeth and may not help with joint pain. For more serious cases of joint pain, a referral to a TMJ specialist may be necessary to determine further treatment.
Impaction & eruption
Dental pain can come from teeth that are erupting (tooth growing out or "cutting") or are impacted (tooth has failed to emerge into its proper position and remains under gum and/or bone). When a molar (the large teeth at the back of the jaw) tooth erupts, the surrounding gum can become inflamed and swollen. Impacted teeth cause pain when they put pressure onto other teeth or bone and are inflamed and/or infected. Treatment for impacted teeth is usually pain medication, antibiotics (for infections), and surgical removal. This most commonly occurs with impacted molar (wisdom) teeth.

Toothache At A Glance

The most common cause of a toothache is a dental cavity.
The second most common cause of toothache is gum disease.
A toothache can be caused by a problem that does not originate from a tooth or the jaw.

REFERENCE:

Davidson, Terence M. "Consultation for Temporal Mandibular Joint Disease (TMJ)." Oct. 10, 2010. University of California, San Diego. <http://health.ucsd.edu/specialties/surgery/davidson/consults/tmj.htm>.

Additional resources from WebMD Boots UK on Toothache Treatment

Source:Medicinenet.com.

Insulin Resistance

2012-03-17T04:34:00.001-07:00

What is insulin resistance?

Insulin is a hormone that is produced by the beta cells, which are cells that are scattered throughout the pancreas. The insulin produced is released into the blood stream and travels throughout the body. Insulin is an important hormone that has many actions within the body. Most of the actions of insulin are directed at metabolism (control) of carbohydrates (sugars and starches), lipids (fats), and proteins. Insulin also is important in regulating the cells of the body including their growth.
Insulin resistance (IR) is a condition in which the cells of the body become resistant to the effects of insulin, that is, the normal response to a given amount of insulin is reduced. As a result, higher levels of insulin are needed in order for insulin to have its effects. The resistance is seen with both the body's own insulin (endogenous) and if insulin is given through injection (exogenous).

What causes insulin resistance?

There are probably several causes of insulin resistance and there is thought to be a strong genetic factor (an inherited component), Some medications also can lead to insulin resistance. In addition, insulin resistance is seen often in the following conditions:

the metabolic syndrome
obesity
pregnancy
infection or severe illness
stress
during steroid use

What is the relationship between insulin resistance and diabetes?

Type 2 diabetes is the type of diabetes that occurs later in life. Insulin resistance precedes the development of type 2 diabetes, sometimes by years. In individuals who will ultimately develop type 2 diabetes, it is believed that blood glucose and insulin levels are normal for many years; then at some point in time, insulin resistance develops.
At this point, there is often an association of high insulin levels, central obesity, cholesterol abnormalities, and /or high blood pressure (hypertension). When this constellation of disease processes occur, it is know as the metabolic syndrome.
One of the actions of insulin is to cause the cells of the body, particularly the muscle and fat cells, to remove and use glucose from the blood. This is one way in which insulin controls the level of glucose in blood. Insulin has this effect on the cells by binding to insulin receptors on the surface of the cells. You can think of it as insulin "knocking" on the doors of muscle and fat cells. The cells hear the knock, open up, and let glucose in to be used by the cell. With insulin resistance, the muscles don't hear the knock as well (they are resistant), and the pancreas is notified that it needs to make more insulin, which increases the level of insulin in the blood and causes a louder knock.
The resistance of the cells continues to increase over time. As long as the pancreas is able to produce enough insulin to overcome this resistance, blood glucose levels remain normal. When the pancreas can no longer produce enough insulin, the blood glucose levels begin to rise, initially after meals when glucose levels are at their highest and more insulin is needed, but eventually in the fasting state too. At this point, type 2 diabetes is present.

What medical conditions are associated with insulin resistance?

While the metabolic syndrome links insulin resistance with abdominal obesity, elevated cholesterol and high blood pressure, there are several medical other conditions that are associated with insulin resistance specifically. It may be that insulin resistance is the cause of some of these conditions, but this has not yet been proven. Conditions associated with insulin resistance include:
Type 2 Diabetes
Overt diabetes may be the first sign that insulin resistance is present. While it can be noted long before diabetes develops, in cases where there is reluctance or inability to see a physician regularly, insulin resistance can present as type 2 diabetes.
Fatty liver
Fatty liver is strongly associated with insulin resistance. The accumulation of fat in the liver is a manifestation of the disordered control of lipids that occurs with insulin resistance. Fatty liver associated with insulin resistance may be mild or severe. Newer evidence suggests that fatty liver may even lead to cirrhosis of the liver and, possibly, liver cancer.
Arteriosclerosis
Arteriosclerosis, also known as atherosclerosis, is a process of progressive thickening and hardening of the walls of medium-sized and large arteries. Arteriosclerosis is responsible for:

coronary artery disease (angina and heart attack ),
strokes and
peripheral vascular disease.

Other risk factors for arteriosclerosis include:

high levels of "bad" (LDL) cholesterol,
high blood pressure,
smoking,
diabetes, and a
family history of arteriosclerosis.

Skin Lesion
Skin lesions include increased skin tags and a condition called acanthosis nigricans - a darkening and thickening of the skin especially in fold areas such as the neckline and axilla. This condition is directly related to the insulin resistance, though the exact mechanism is not known.

Acanthosis nigricans: Acanthosis nigricans is a cosmetic condition strongly associated with insulin resistance in which there is darkening of the skin in areas where there are creases such as the neck and arm pits.
Skin tags: Skin tags are also seen with increased frequency in patients with insulin resistance. A skin tag is a common, benign condition which consists of a bit of skin that projects from the surrounding skin and may appear attached to the skin. Skin tags can vary quite a bit in appearance. They may be smooth or irregular, flesh colored or more deeply pigmented, and either simply be raised above the surrounding skin or have a stalk (a peduncle) so that the skin tag hangs from the skin.

Reproductive abnormalities in women
Reproductive abnormalities include difficulty with ovulation and conception (infertility), irregular menses, or a cessation of menses. In contrast, there are no known reproductive abnormalities in men with insulin resistance.
Polycystic ovary disease
Polycystic ovary disease is a hormonal problem that affects young women. It is associated with irregular periods or no periods at all, obesity, and increased growth of body hair.
Hyperandrogenism
High male hormone levels, which are produced by the ovaries can been seen in insulin resistance and may play a role in PCOS described above. Why this association occurs is not known, but it's thought that the insulin resistance somehow causes the abnormal ovarian hormone production.
Growth abnormalities
There may be growth affects in insulin resistance due to the high levels of circulating insulin that may be present. While insulin's effects on glucose metabolism may be impaired, it's effects on other mechanisms may be intact (or at least less impaired). Insulin is an anabolic and can exert effects on growth, through a medicator known as insulin- like growth factor -1. Patients may have actual linear growth and a noticeable coarsening of features. The increase incidence of skin tags mentioned above may be through this mechanism as well.

Who is at risk for insulin resistance?

Individuals are more likely to have or develop insulin resistance if they:

are overweight with a body mass index (BMI) more than 25
are a man with a waist more than 40 inches or a woman with a waist more than 35 inches
are over 40 years of age
are Latino, African American, Native American or Asian American
have close family members with type 2 diabetes, high blood pressure or arteriosclerosis
have had gestational diabetes
have high blood pressure, high blood triglycerides, low HDL cholesterol or arteriosclerosis (for example, have other components of the metabolic syndrome)
have polycystic ovarian disease
have acanthosis nigricans

How is insulin resistance diagnosed?

A physician can identify individuals who are likely to have insulin resistance with a detailed patient history, patient physical examination, and laboratory testing utilizing the risk factors. There are some very sophisticated tests for the diagnosis or confirmation of insulin resistance such as euglycemic insulin clamping or intravenous tolerance testing. However, these are expensive or complicated and are not necessary for managing patients. These tests are used primarily for research purposes.
In general clinical practice, glucose levels in conjunction with fasting insulin levels can give the physician a clue as to whether insulin resistance is present or not in patients without diabetes. A firm diagnosis can not be made simply based on this, since the lab techniques for measuring insulin can vary, and there is no absolute value that meets a definition. However, a level above the upper quartile in the fasting state in someone without diabetes is considered abnormal.

How is insulin resistance managed?

Insulin resistance can be managed in two ways. First, the need for insulin can be reduced, and second, the sensitivity of cells to the action of insulin can be increased.
Life-style changes
The need for insulin can be reduced by altering the diet, particularly the carbohydrates in the diet. Carbohydrates are absorbed into the body after they are broken up into their component sugars. Some carbohydrates are broken up and absorbed faster than others and are referred to as having a high glycemic index. These carbohydrates increase the blood glucose level more rapidly and require the secretion of more insulin to control the level of glucose in the blood.
Examples of carbohydrates with a high glycemic index that rapidly raise blood glucose levels include:

unrefined sugars,
white breads, and
unrefined corn and potato products (for example, bagels, mashed potatoes, doughnuts, corn chips, and french fries).

Examples of foods with a low glycemic index include:

foods with higher fiber content such as whole grain breads and brown rice;
non-starchy vegetables (for example, broccoli, green beans, asparagus, carrots, and greens).

Since foods are rarely eaten in isolation, it can be argued that the glycemic index of each food isn't as important as the overall profile of the whole meal itself.
Several studies have shown that weight loss and aerobic exercise (without weight loss) increase the rate at which glucose in the blood is taken up by muscle cells as a result of improved sensitivity of the cells to insulin.
There are two important studies that have looked at the prevention of type 2 diabetes. Both studies took patients who could not control their blood glucose levels, which, for the purposes of this discussion, can be considered the same as patients with insulin resistance. One study done in Finland, showed that changes in diet and exercise reduced the development of diabetes by 58%. Another study, done in the United States and referred to as the DPP study, showed a similar reduction in diabetes with diet and exercise.
Medications
Metformin (Glucophage) is a medication that is used for treating diabetes. It has two mechanisms of action that help to control blood glucose levels. It prevents the liver from releasing glucose into the blood, and it increases the sensitivity of muscle and fat cells to insulin so that they remove more glucose from the blood. Because of these actions, metformin reduces blood insulin levels.
The DPP studied the effects of metformin in addition to diet and exercise on the prevention of diabetes in insulin resistance. Metformin reduced the development of diabetes by 31%. (Note, however, that the benefit was not as great as with diet and exercise!) Metformin is a reasonably safe medication when used in the right population. Although there are gastrointestinal side effects with metformin, it usually is well-tolerated.
Another study, the STOP NIDDM (Study to Prevent Non-insulin Dependent Diabetes Mellitus) trial, studied individuals with insulin resistance by treating them with a medication called acarbose (Precose). Acarbose works in the intestines to slow the absorption of sugars, and this effect would reduce the need for insulin after meals. The study found that acarbose reduced the development of diabetes by 25%.
Other medications in a class of drugs called thiazolidinediones, for example, pioglitazone (Actos), rosiglitazone (Avandia), also increase sensitivity to insulin. At this time, however, these medications are not routinely used, in part because of liver toxicity that requires monitoring of blood liver tests. Avandia, however, has been associated with an increased risk of heart attack and stroke, and experts have debated the severity of these concerns since the risk was first reported. On September 23, 2010, the U.S. Food and Drug Administration (FDA) announced that it will significantly restrict the use of the diabetes drug rosiglitazone (Avandia) to patients with type 2 diabetes who cannot control their diabetes on other medications such as pioglitazone (Actos). These new restrictions are in response to data that suggest an elevated risk of cardiovascular events, such as heart attack and stroke, in patients treated with Avandia.
One study, the TRIPOD (Troglitazone in Prevention of Diabetes) study, treated patients with gestational diabetes, a precursor of insulin resistance and diabetes, with troglitazone (Rezulin), however, because of severe toxic liver effects; troglitazone has been taken off the market and is no longer available. Among the women treated with troglitazone, diabetes was prevented in 25%.

What's new in insulin resistance?

It is only in recent years that insulin resistance has been gaining importance its own right, and as a contributor to the metabolic syndrome. It now appears that intervention can delay the onset of overt diabetes. Future studies will need to be longer than the studies already done to determine for how long treatment can prevent the development of diabetes and its complications.
Lifestyle changes (for example, diet, exercise) clearly are important in delaying the development of diabetes in individuals with insulin resistance, and education about these changes needs to be directed to groups at risk for diabetes. Childhood obesity is on the rise in the United States as well as other countries, and changes need to be made in school cafeterias and in the food choices offered to children and teens at home.
The value of diet and exercise in combination with medication needs to be evaluated to determine if the combination is better than diet and exercise alone.

Insulin Resistance At A Glance

Insulin resistance is a condition in which the cells of the body become resistant to the hormone, insulin.
Insulin resistance may be part of the metabolic syndrome, and associated with the development of heart disease.
Insulin resistance precedes the development of type 2 diabetes.
Insulin resistance is associated with other medical conditions including fatty liver, arteriosclerosis, acanthosis nigricans, skin tags, and reproductive abnormalities in women.
Individuals are more likely to have insulin resistance if they have any of the associated medical conditions listed above. They also are more likely to be insulin resistant if they are obese or are Latino, African-American, Native American, and Asian-American.
While there is a genetic component, insulin resistance can be managed with diet, exercise, and medication.

REFERENCE: FDA Prescribing Information for Avandia.

Source:Medicinenet.com.

Medical Author:

Ruchi Mathur, MD, FRCP(C)

Medical Author:

Melissa Conrad Stöppler, MD

Medical Editor:

Jay W. Marks, MD

Medical Editor:

William C. Shiel Jr., MD, FACP, FACR

Secondhand Smoke

2012-03-17T04:31:00.001-07:00

What is secondhand smoke?

Secondhand smoke refers to tobacco smoke that is passively breathed in by people in the vicinity of a person who is smoking. Terms that have been used to refer to secondhand smoke are passive smoking, involuntary smoking, or environmental tobacco smoke (ETS). Secondhand smoke is a mixture of the smoke from the tobacco product itself (termed sidestream smoke) and exhaled smoke from the smoker (known as mainstream smoke).
When a nonsmoker inhales secondhand smoke, he or she is exposed to the same toxins and chemicals, including nicotine, as the smoker.
Exposure of children to secondhand smoke also increases their health risks; and children are especially vulnerable to the effects of environmental tobacco smoke. About 35% of U.S. children live in homes where smoking occurs regularly. Research has shown that 50% to 75% of children in the U.S. have detectable levels of cotinine (the breakdown product of nicotine) in their blood, so even children who do not live with smokers may be at risk for adverse effects of secondhand smoke. Chemicals from tobacco smoke inhaled by a nursing mother are also known to reach breast milk.

What causes secondhand smoke?

Cigarettes are the most common sources of secondhand smoke, followed by cigars and pipe smoke. People can be exposed to environmental tobacco smoke anywhere - in their homes, in the workplace, and in recreational settings.

What are the health risks of secondhand smoke?

Secondhand smoke carries many health risks. At least 250 harmful chemicals have been identified in secondhand smoke, including at least 50 carcinogens (chemicals that are known to cause cancer). Just some of the dangerous chemicals present in secondhand smoke include vinyl chloride, cadmium, benzene, arsenic, and ethylene oxide.
Secondhand smoke is known to cause cancer. It has been classified as a "known human carcinogen" by the U.S. Environmental Protection Agency (EPA). It is also associated with cardiovascular and respiratory diseases as well as other serious health conditions; several are listed below.

Lung cancer and secondhand smoke

Passive smoking is an established risk factor for the development of lung cancer. Research has shown that nonsmokers who reside with a smoker have a 20% to 30% increase in risk for developing lung cancer when compared with nonsmokers who do not reside with a smoker. An estimated 3,400 lung cancer deaths that occur each year in the U.S. are attributable to passive smoking.

Cardiovascular disease and secondhand smoke

Like cigarette smoking itself, secondhand smoke is a significant risk factor for the development of cardiovascular disease and heart attack. An estimated 46,000 deaths from heart disease in non-smokers who live with smokers occur every year in the U.S.

Other lung diseases and secondhand smoke

Coughing, chest congestion, and decreased lung function can also occur in those exposed to passive smoke. Babies exposed to secondhand smoke can also develop serious respiratory infections. In the U.S., passive smoking is believed to cause 150,000 to 300,000 lung infections (such as pneumonia and bronchitis) in children younger than 18 months of age each year.

Secondhand smoke and other effects on children

In addition to the risk of pneumonia and respiratory infections in babies exposed to secondhand smoke (see above), passive smoke is known to increase the severity of asthma in children with this condition. About 750,000 middle ear infections in children are also estimated to occur each year as a result of exposure to secondhand smoke. Babies who are exposed to secondhand smoke are at an increased risk for sudden infant death syndrome (SIDS).

Secondhand smoke and the effects on pregnant women

Like women who smoke, pregnant women who are exposed to secondhand smoke have an increased risk of having low-birthweight babies.

Secondhand smoke and the possible link to breast cancer

The question of whether or not passive smoking is associated with an increased risk of breast cancer is currently a source of both investigation and controversy. Breast cancer risk in active smokers is not known to be increased, yet some studies have found a possible link to breast cancer with exposure to passive smoke. In 2006, the U.S. Surgeon General's report concluded that there is "suggestive but not sufficient" evidence of a link at this point.

Is there a safe level of secondhand smoke?

While, logically, more extensive or prolonged exposure to secondhand smoke, is associated with greatest risk of having medical problems as a result, no safe limit for exposure to secondhand smoke has been established. Even low levels of secondhand smoke can be harmful. This means that all exposure to secondhand smoke should be avoided whenever possible.

What can be done about secondhand smoke exposure?

Local, state, and national governments have enacted a variety of laws designed to protect people from health dangers associated with secondhand smoke. These laws vary according to location. The American Lung Association has a listing of these regulations grouped by U.S. state (see References below). Legislation to prevent smoking in workplaces and public buildings is on the rise as the public becomes more informed about the risks of secondhand smoke.
Obviously, quitting smoking if you are a smoker is the best way to protect your family and friends from secondhand smoke. A number of support systems, programs, and even prescription medications are available to help smokers break the habit.
If you are a non-smoker, the safest way to avoid passive smoke is not to allow others to smoke in your home. This is particularly important if there are children in your home. According to the U.S. Surgeon General, smoke-free workplaces are the only way to protect people from exposure to secondhand smoke in the workplace, since separate smoking areas, cleaning the air, and ventilating the building are not sufficient to prevent exposure if people still are permitted to smoke inside the building.

What is thirdhand smoke?

Thirdhand smoke exposure is a new concept; it is exposure to many of the toxic agents in smoke that have accumulated (as residue) in clothing, drapes, rugs, furniture, dust, and other items due to secondhand smoke. The toxic agents, deposited in and on items from secondhand smoke, can be absorbed through the skin and mucous membranes of non-smokers, especially by infants and young children. Prevention of secondhand smoke exposure can prevent thirdhand smoke exposure.

Secondhand Smoke At A Glance

Secondhand smoke refers to tobacco smoke that is passively breathed in by people in the vicinity of a person who is smoking.
Secondhand smoke causes significant health problems, including cancer.
Children are particularly vulnerable to secondhand smoke, experiencing an increase in lung infections, bronchitis, worsening of asthma, and increased risk for SIDS.
Legislation to prevent smoking in workplaces and public buildings is on the rise as the public becomes more informed about the risks of secondhand smoke.

American Cancer Society. "Secondhand Smoke."
<http://www.cancer.org/docroot/PED/content/PED_10_2X_Secondhand_Smoke-Clean_Indoor_Air.asp>

American Lung Association. "Smoking restrictions in U.S. States."
< http://slati.lungusa.org>

National Cancer Institute. "Secondhand Smoke."
< http://www.cancer.gov/cancertopics/factsheet/Tobacco/ETS>

Sleiman, M., Gundel, L., Pankow, J., et al. "Formation of carcinogens indoors by surface-mediated reactions of nicotine with nitrous acid, leading to potential thirdhand smoke hazards." PNAS; doi:10.1073/pnas.0912820107

Source:Medicinenet.com.

Medical Author:

Melissa Conrad Stöppler, MD

Medical Editor:

Charles Patrick Davis, MD, PhD

Fatigue

2012-03-17T04:30:00.001-07:00

Fatigue Facts

Fatigue (either physical, mental or both) is a symptom that may be difficult for the patient to describe and words like lethargic, exhausted and tired may be used.
Taking a careful and complete history is the key to help making the underlying diagnosis of the cause for the symptom of fatigue, However, in about a third of patients the cause is not found and the diagnosis is not known.
There are numerous causes of fatigue symptoms. Examples of some treatable causes of fatigue include anemia, diabetes, thyroid disease, heart disease, COPD and sleep disorders (Table).
Long lasting complaints of fatigue does not equate to chronic fatigue syndrome. Specific criteria as set by the CDC need to be met to make that particular diagnosis.

Fatigue introduction

Fatigue can be described as the lack of energy and motivation (both physical and mental). This is different than drowsiness, a term that describes the need to sleep. Often a person complains of feeling tired and it is up to the health care professional to distinguish between fatigue and drowsiness, though both can occur at the same time. Aside from drowsiness, other symptoms can be confused with fatigue including shortness of breath with activity and muscle weakness. Again, all these symptoms can occur at the same time. Also, fatigue can be a normal response to physical and mental activity; in most normal individuals it is quickly relieved (usually in hours to about a day, depending on the intensity of the activity) by reducing the activity.
Fatigue is a very common complaint and it is important to remember that it is a symptom and not a disease. Many illnesses can result in the complaint of fatigue and they can be physical, psychological, or a combination of the two.
Often, the symptom of fatigue has a gradual onset and the person may not be aware of how much energy they have lost until they try to compare their ability to complete tasks from one time frame to another. They may presume that their fatigue is due to aging and ignore the symptom. This may lead to a delay in seeking care.
While it is true that depression and other psychiatric issues may be the reason for fatigue, it is reasonable to make certain that there is not an underlying physical illness that is the root cause.
Individuals with fatigue may have three primary complaints; however, it can vary in each person.

There may be lack of motivation or the ability to begin an activity;
the person tires easily once the activity has begun; and
the person has mental fatigue or difficulty with concentration and memory to start or complete an activity.

While fatigue can last for a prolonged period of time, the presence of chronic fatigue is different than chronic fatigue syndrome, which has specific set of two criteria set for by the Centers for Disease Control and Prevention as follows:

Have severe chronic fatigue for at least six months or longer with other known medical conditions (whose manifestation includes fatigue) excluded by clinical diagnosis; and
Concurrently have four or more of the following symptoms:

post-exertional malaise
impaired memory or concentration
unrefreshing sleep
muscle pain
multi-joint pain without redness or swelling
tender cervical or axillary lymph nodes
sore throat
headache

Other words that a person might use to describe fatigue may include the following:

lethargic,
listless,
lack of energy,
tired,
worn out,
weary,
exhausted,
malaise, or
feeling run down.

What causes fatigue?

There are numerous potential causes of fatigue as a major complaint. They range from those that cause poor blood supply to the body's tissues to illnesses that affect metabolism, from infections and inflammatory diseases to those that cause sleep disturbances. Fatigue is a common side effect of many medications. While numerous patients with psychological conditions often complain of fatigue (physical and mental), there are also a group of patients where the cause of fatigue is never diagnosed.
The following table summarizes some common causes of fatigue but is not meant to be comprehensive:

Common Causes of Fatigue
Metabolic/ Endocrine	Anemia; Hypothyroidism; Diabetes; Electrolyte abnormalities; Kidney disease; Liver disease; Cushing's disease
Infectious	Infectious mononucleosis; Hepatitis; Tuberculosis; Cytomegalovirus; HIV infection; Influenza (flu); Malaria and many other infectious diseases
Cardiac (heart) and Pulmonary (lungs)	Congestive heart failure; Coronary artery disease; Valvular heart disease; COPD; Asthma; Arrythmias; Pneumonia
Medications	Antidepressants; Anti-anxiety medications; Sedative medications; Medication and drug withdrawal; Antihistamines; Steroids; Some blood pressure medications; Some antidepressants
Psychiatric (Mental Health)	Depression; Anxiety; Drug abuse; Alcohol abuse; Eating disorders (for example; bulimia; anorexia); Grief and bereavement
Sleep Problems	Sleep apnea; Reflux esophagitis; Insomnia; Narcolepsy; Work shift work or work shift changes; Pregnancy; Extra night hours at "work"
Other	Cancer; Rheumatology illnesses such as rheumatoid arthritis and systemic lupus; Fibromyalgia; Chronic fatigue syndrome; Normal muscle exertion; Obesity; Chemotherapy and radiation therapy

What are the signs and symptoms of fatigue?

Fatigue is a symptom of an underlying disease and is described in many ways from feeling weak to being constantly tired or lacking energy.
There may be other associated symptoms depending upon the underlying cause.

Individuals with heart disease, lung disease, or anemia may complain of associated shortness of breath or tiring easily with minimal activity.
Persons with diabetes may complain of polyuria (excess urination), polydypsia (excess thirst), or change of vision.
Those who have hypothyroidism may also have symptoms of feeling cold, dry skin and brittle hair.

It is important that the health care practitioner consider the complaint of fatigue in the context of the whole patient to try to come to an accurate causative diagnosis.

How is the cause of fatigue diagnosed?

The key to finding the cause of fatigue in a patient is the care the health care practitioner takes in compiling a medical history. It is important to ask questions not only about the loss of energy but also about other potential problems that the patient may be experiencing such as shortness of breath, sleep patterns, hair loss, color of the stools, or any of the myriad of questions that might provide information as to what organ system may be involved.
Usually, a history is taken by the health care practitioner asking questions about the quality and quantity of fatigue. Examples of some of the questions the health care practitioner may ask include:

Does the patient feel well in the morning when they wake?
Does the fatigue progress through the day?
Does the person nap unexpectedly or take excessive amounts of stimulants such as caffeine to complete daily activities?
Does the fatigue come on gradually or abruptly?
Is it a daily occurrence or intermittent/periodic?
What makes it better and what makes it worse?
How has the patient's life changed because of the fatigue?
Is the fatigue more mental than physical?

Other associated symptoms with fatigue include:

weight loss,
chest pain and shortness of breath,
vomiting and diarrhea,
fevers and chills,
muscle weakness or pain, and/or
anxiety and depression.

It is also appropriate for the health care practitioner to ask questions about the patient's social situation and to also ask about their psychologic state of mind. Alcohol and drug abuse screening questions should be expected as routine.
Because fatigue is such a non-specific symptom, each answer may direct the health care practitioner to explore a different potential cause.
A full physical examination is important to look for underlying signs of illness. The general appearance of the patient is important looking for hygiene, vital signs, and evidence of anxiety or agitation. Examination and evaluation of the different systems of the body (heart, lungs, abdomen, neurological system, etc.) and combining any abnormal findings with the clues found in the history taking may help make the diagnosis.
Special attention may be taken to palpate (feel) for an abnormal thyroid gland, swollen lymph nodes, listen for abnormal heart sounds including murmurs and to check for normal muscle tone and reflexes.
Depending on the findings in the history and physical examination, blood tests and other imaging studies may be ordered. Initial screening blood tests may include:

CBC (complete blood count that includes a red blood cell, white blood cell and platelet count);
electrolytes (sodium potassium, chloride, carbon dioxide, and sometimes calcium and magnesium);
glucose (blood sugar);
BUN/creatinine (to measure kidney function);
TSH or thyroid stimulating hormone;
CPK (elevated in illnesses that cause muscle inflammation); and/or
ESR or erythrocyte sedimentation rate (non specific blood marker for inflammation in the body).

The decision to obtain X-rays, CT scans, electrocardiogram (ECG, EKG) and other imaging or testing will depend upon the individual patient's circumstances and what the health care practitioner suspects may be the underlying cause of the fatigue.

What is the treatment for fatigue?

Since fatigue is a symptom of an underlying condition, the treatment depends upon the condition that is causing the fatigue, regardless of whether it is physical, psychological or a combination of the two.
There may be a lag time between when the illness has been treated and the intensity of fatigue symptoms; some symptoms may resolve as soon as the underlying condition is treated. For example, individuals who are anemic feel much better as soon as their red blood cell count increases, while those recovering from infectious mononucleosis may require weeks to have their energy levels return to normal.

Can fatigue be prevented?

Fatigue as a symptom can occur as the result of many causes and therefore, prevention is not an issue. More importantly, the early recognition of fatigue will allow a person to seek medical care and potentially have an earlier diagnosis of the underlying cause made.
Sometimes, symptoms like fatigue arise gradually and it is difficult for the person to realize that there is a problem. It may take an outside perspective from a friend or family member to appreciate a difference in function. Self-awareness of gradual decline in body performance is often difficult as a person makes repeated small accommodations to complete daily activities.

REFERENCES:

Centers for Disease Control and Prevention. Chronic Fatigue Syndrome.
<http://www.cdc.gov/cfs/>

Davis, Mp., Walsh, D. Mechanisms of fatigue, J. Support. Oncol., 8:164-174, 2010

MedlinePlus.com. Fatigue.
<http://www.nlm.nih.gov/medlineplus/ency/article/003088.htm>

Medical Author:

Benjamin Wedro, MD, FACEP, FAAEM

Medical Editor:

Charles Patrick Davis, MD, PhD
Source:Medicinenet.com.

Pregnancy Planning

2012-03-17T04:28:00.001-07:00

Pregnancy Planning Facts

Pregnancy planning can address issues of nutrition, vitamins, body weight, exercise, and potentially harmful medications and illnesses as well as immunizations and genetic counseling.
Women who take folic acid at least four weeks prior to conception can reduce their baby's risk of birth defects of the spinal cord and skull by 70%.
Alcohol has been implicated in infertility, early miscarriage, and birth defects.
Certain acne medications and other prescription and OTC medications can cause birth defects.
Babies of older women have an increased risk of having chromosomal abnormalities.
The timing of sexual intercourse in relation to ovulation does not influence the gender of the baby.

What is pregnancy planning and why is it important?

Having a baby is one of the most important events in a woman's life. Women considering pregnancy are encouraged to start planning for the pregnancy with their doctors early. This early planning process is called pregnancy planning. The goals of pregnancy planning are to create a healthy environment for the fetus and to prevent birth defects and other pregnancy related problems to the greatest extent possible. The issues addressed during pregnancy planning include nutrition, vitamins, body weight, exercise, avoidance of certain medications and alcohol, immunizations, and genetic counseling. Even though many women will have normal pregnancies without any planning, pregnancy planning improves the chances of a smooth pregnancy and a healthy baby. Unfortunately, many more women who are anticipating conceiving do not seek prior medical consultation.
Pregnancy planning can help prevent exposure of the mother to potentially harmful medications or substances during the early days of pregnancy. The baby's organs begin developing as early as 17 days after conception, and the fertilized egg begins to grow even before the first day of the missed period. Some women continue to have light bleeding that may be mistaken for a menstrual period during the first few months of pregnancy and may not even realize that they are pregnant. Others may not recognize that they are pregnant until they experience weight gain or abdominal enlargement. By then, they may have already been exposed to medications or substances potentially harmful to the fetus.
In addition to avoiding medications and substances that are potentially harmful to the fetus, other important health issues are addressed during pre-pregnancy planning.

Conditions such as diabetes, high blood pressure, kidney disease, thyroid disease, and heart disease in the mother are controlled to optimize pregnancy outcome.
The status of the woman's immunity against German measles (rubella) and varicella (chickenpox) is also determined. Women lacking rubella antibodies are immunized before conceiving (see medical issues below). Women who are not immune to varicella (chickenpox) can be vaccinated, but should wait 30 days after vaccination before becoming pregnant.
Women who are carriers of the hepatitis B virus can be identified by blood tests, and their infants can be protected from hepatitis B infection by immunizations at the time of delivery. Women with HIV (human immunodeficiency virus) infection should take certain medications during pregnancy to decrease not only their risks but those of the fetus as well.

The effects of diet, exercise, and each of the medical conditions previously discussed will be reviewed below.

What are pregnancy symptoms?

There are both symptoms and signs of pregnancy. These symptoms and signs depend upon the time in pregnancy. In the first trimester of pregnancy, the first sign of pregnancy is most often a missed menstrual period. If a sexually active woman's periods are generally regular, missing a period for a week or more is presumptive evidence of pregnancy.
Early symptoms of pregnancy also include feelings of breast swelling and tenderness, and nausea sometimes with vomiting. "Morning sickness" does not always occur in the morning, and the nausea of pregnancy can occur at any time of day. Many women become fatigued early in pregnancy, and some may feel abdominal enlargement (bloating).
Early in pregnancy, the woman may feel she has to urinate frequently, especially at nighttime, and she may leak urine when coughing, sneezing or laughing. This is also normal later in pregnancy and is not a problem.
Other changes characteristic of pregnancy include the deepening color of the areola (area surrounding the nipple), increased body temperature, the so-called "mask of pregnancy" (darkening of skin on the forehead, bridge of the nose, or cheekbones), and a dark line going down from the middle of the central abdomen area to the pubic area. Eventually, enlargement of the abdomen is a normal feature of the growing fetus.

What is a pregnancy calculator and calendar?

A pregnancy calendar or calculator can allow a pregnant woman to understand what is happening to her body and to the developing embryo or fetus at each stage of pregnancy. Most pregnancy calendars explain the changes of pregnancy on a week-to-week level and can be found online or in print form. In many cases, pregnancy calendars contain photos or diagrams to illustrate the appearance of the fetus at each stage.

How effective are home pregnancy tests?

At-home pregnancy tests, first introduced in 1975, are very accurate and reliable when used correctly. These tests measure the presence of the hormone human chorionic gonadotropin in the urine, which, when present, is indicative of pregnancy. The same hormone is measured in blood and urine pregnancy tests available at clinics and doctors' offices. Currently, the blood test is the most specific and sensitive pregnancy test available, although urine tests have become increasingly sensitive. For example, home urine tests may be able to detect the pregnancy hormone at 8 to 9 days after conception, or a few days before the missed menstrual period.
While many manufacturers claim that their home pregnancy tests are 99% accurate, a number of factors influence the accuracy of these kits. Studies have shown that false negative results may occur when very low levels of the pregnancy hormone are present, and that home test kits from different manufacturers differ in their sensitivity for detection of the very low levels of the pregnancy hormone in the early days of pregnancy. If a woman takes a home pregnancy test too soon, the result may be negative even though she is in the first stages of pregnancy. A repeat test should always be performed a week later if a home test is negative and a woman suspects that she might be pregnant.

How can diet and nutrition affect early pregnancy?

The developing fetus receives its nutrition from the mother's blood. Therefore high fat diets and some vegetarian diets are discouraged during pregnancy because they may not provide all the nutrition needed for the developing fetus. Bulimia, anorexia nervosa and other eating disorders in the mother are addressed and treated. Weight reduction diets are avoided during pregnancy. Excess intake of sugar, alcohol, megavitamins, and caffeine are also avoided Because a "safe" amount of caffeine has never been confirmed to date, it is best to avoid caffeine entirely. Women who feel strongly that they need some coffee are advised to drink no more than one cup per day. There is no proof that 1 to 2 cups of coffee daily cause pregnancy complications.
Listeria is a type of bacteria found in contaminated food that can cause miscarriage and other problems in a fetus. Because of the danger of getting a listeria infection, pregnant women should avoid unpasteurized milk, soft cheeses, cold cuts, and undercooked or raw animal foods. In addition, fruits and vegetables should be washed completely prior to consumption.
Phenylketonuria is an inherited disease that affects the utilization of a certain protein component in foods. This disorder can be detected by a blood test. Mothers with phenylketonuria may give birth to developmentally disabled children unless their diets are strictly controlled to exclude phenylalanine.
Megavitamins contain double or even triple the recommended daily allowances of vitamins and minerals. High doses of vitamin A have been implicated in producing birth defects. The better idea is to avoid megavitamins and instead follow the recommendation that has proven benefit: take a prenatal vitamin containing folic acid.
Folic acid intake in the mother prior to, and during pregnancy has been shown to reduce the risk of birth defects involving the brain and spinal cord. The United States Public Health Service recommends folic acid for all women of child-bearing capacity. Studies have shown that if folic acid is begun at least 4 weeks prior to conception, the risk of birth defects of the spinal cord and skull can be reduced by more than 70%. In women with or even without a history of having infants with birth defects of the spinal cord or skull, folic acid should be taken one month before conception and continued through the 12th week of pregnancy. In fact, continuing prenatal vitamins through pregnancy and even through nursing is probably wise. These prenatal vitamins are available over-the-counter. If a particular brand makes you feel nauseated, simply switch to another brand or try taking the vitamin at night.
Because of the risks of mercury poisoning and nervous system damage in the fetus from contaminated fish, pregnant women are advised to eliminate consumption of certain types of fish that are known to be high in mercury, including shark, swordfish, tilefish, and king mackerel. Tuna steaks, made from large tuna, may also have high mercury levels. Canned tuna is made from smaller fish that typically have lower levels of mercury than larger fish.

How does alcohol affect pregnancy?

Alcohol has been implicated in infertility, early miscarriage, as well as in birth defects. The amount of alcohol consumption necessary to cause these problems is not known, and varies among women. Some women can drink excessively and have normal infants. Others consume considerably less alcohol but still give birth to babies with cognitive disabilities and/or other birth defects. It is generally believed that the greater the amount of alcohol consumed during pregnancy, the greater the risk of pregnancy-related problems and birth defects.
It is recommended that pregnant women avoid all consumption of alcohol. Fetal alcohol spectrum disorders are a group of conditions reflecting the possible effects of prenatal exposure to alcohol. The FASDs include fetal alcohol syndrome (FAS), alcohol-related birth defects (ARBD), and alcohol-related neurodevelopmental disabilities (ARND). Fetal alcohol syndrome (FAS) is the extreme end of the fetal alcohol spectrum disorders and is a leading cause of cognitive disabilities.

How do high blood pressure and diabetes affect pregnancy?

Elevated blood pressure (hypertension) that is present before pregnancy can interfere with growth of the fetus and increase the risk of fetal death. Therefore, controlling blood pressure with carefully chosen blood pressure medications is important during pregnancy and before conception.
In addition, underlying hypertension can increase the risk for a condition called preeclampsia, a potentially very dangerous complication of pregnancy. It is sometimes difficult for doctors to distinguish between high blood pressure alone and high blood pressure occurring from preeclampsia. For those reasons, and given the risk of birth defects from many of the blood pressure medications, women with high blood pressure who become pregnant should be followed very carefully by a medical expert who is familiar with this type of situation. Ideally, medication would be switched to a relatively safe medication before the woman even becomes pregnant.
Poorly controlled diabetes can lead to high blood sugar levels. High blood sugar levels during early pregnancy can lead to miscarriages and birth defects. Therefore, controlling diabetes is important for a good pregnancy outcome, and the blood sugar should ideally be controlled before becoming pregnant. It is important to consider that control of blood sugar during pregnancy is important, but control prior to pregnancy may be just as important.
Oral diabetes medications may be dangerous to the fetus, but insulin is not dangerous to the fetus. Insulin is the key treatment for diabetes during pregnancy. Not only is insulin safe to the baby and mother, but it also helps prevent the complications that the baby could have suffered from the mother's sugar being uncontrolled. Insulin is usually substituted for pills as soon as a woman with diabetes is considering pregnancy. The ideal time to control blood sugar is before pregnancy, because control of sugar levels even in early pregnancy (when the mother does not yet know she is pregnant) is important for the developing baby's health.

What are examples of commonly-used medications that are dangerous in pregnancy?

Many women do not know that over-the-counter medications can be dangerous. In fact, many prescription and over-the-counter medications harm the fetus very early in pregnancy at a time that the mother does not even know she is pregnant. Even aspirin use by the mother can cause defects in the fetus. For this reason, as soon as pregnancy is being contemplated, women should avoid all over-the-counter and prescription medications until reviewed with their doctor.
Acne medications, such as isotretinoin (Accutane) can cause birth defects, and should be discontinued before conception. Since many medications and substances can affect fetal growth and development, pregnancy planning is important so that potentially harmful substances can be stopped before conceiving.
Unplanned pregnancy during oral contraceptive use is not felt to pose a significant danger to the fetus, although deliberate use of oral contraceptives during pregnancy is not advisable. Women who become pregnant during oral contraceptive use have the same risk of birth defects in their newborns as the general population of women, in the range of 2% to 3%.

How do kidney and heart disease affect pregnancy?

Because pregnancy is associated with an increase in blood volume and an increase in cardiac output as well as other changes in the circulatory system, many types of heart disease may worsen or be associated with poor outcome during pregnancy. While many mild chronic heart conditions may be well tolerated during pregnancy, other conditions pose a significant risk to mother and fetus. Women with preexisting heart disease should always consult an expert when planning a pregnancy to examine their own degree of risk, potential outcomes, and treatment options.

What infections affect pregnancy?

Certain infections during early pregnancy can cause birth defects in the fetus. Rubella (German measles) virus infection during early pregnancy can cause birth defects and even miscarriages. Therefore, women of child bearing age are tested for blood antibodies against this virus. Women lacking rubella virus antibodies are susceptible to rubella infection, and should be vaccinated against this virus. Pregnancy should be avoided for one month after vaccination, due to the theoretical concern that the vaccine virus itself may cause fetal damage.
Toxoplasmosis is a small parasite that is transmitted through cat feces and raw meats, especially pork. Toxoplasmosis, like the rubella virus, can cause severe birth defects if the infection occurs during early pregnancy. Women planning pregnancy should avoid raw meat and avoid handling the cat litter box. Many people have been exposed to toxoplasmosis without even knowing it. As a result, they develop a protective immunity from the "silent" infection. Women who have a blood test that is positive for toxoplasmosis immunity can be reassured that they will not develop toxoplasmosis complications during pregnancy.
Hepatitis B is the only type of hepatitis that is known to affect the newborn infant.
Female healthcare workers, dental assistants, and others exposed to hepatitis B should receive hepatitis B vaccination to avoid chronic infection by this virus. The majority of hepatitis B virus infections resolve spontaneously without treatment. Patients whose disease resolves completely are no longer contagious. Approximately 10% of hepatitis B virus infections do not resolve, and become chronic. Patients chronically infected with hepatitis B virus may have no symptoms of liver disease early on, but they remain contagious. Over time, chronic hepatitis B infection can lead to liver cirrhosis and/or liver cancer.
Women with chronic hepatitis B infection can transmit the virus to their babies at birth. Babies infected are at risk of developing chronic liver disease, liver cirrhosis, and liver cancer in later life. Currently, infants born to mothers infected with the hepatitis B virus are given both the hepatitis B antibodies and hepatitis B vaccinations at birth for protection. Therefore, pregnant women are often tested for signs of hepatitis B infection, even if they do not have any symptoms or knowledge of past infection. The babies of infected mothers detected in this manner would receive special care at (and after) delivery.
Cytomegalovirus (CMV) is a common viral infection worldwide that often does not produce any symptoms. Women who become infected or have a reactivation of a previous infection during pregnancy may pass the infection along to their babies. Congenital CMV infection is the most common congenital viral infection. Although the majority of infected infants will not have any symptoms, up to 20% will have symptoms that may include an enlarged spleen, jaundice, or rash. Rarely, involvement of many organs may occur resulting in severe illness or disability.
Genital herpes may also result in the passage of the infection to the infant at the time of delivery. The risk of transmission is increased if the genital lesions are from a herpesvirus (HSV) infection acquired during the pregnancy, rather than simply a reactivation of previous disease. HSV infection can have multiple effects in the newborn. Disease may be limited to the eyes, skin and mouth; may be localized to the central nervous system; or may be widespread and involve many organs. Treatment involves administration of antiviral medications to the newborn and supportive care.
Parvovirus B19 is a virus that causes the condition known as Fifth disease, a common mild disease of childhood. Transmission is by droplets in the air (respiratory secretions) or through blood. Pregnant women who have not previously had fifth disease should avoid contact with those who have it because parvovirus B-19 can infect a fetus prior to birth. Although no birth defects have been reported as a result of fifth disease, it can cause the death of an unborn fetus. This occurs in less than 5% of pregnant women who become infected with the virus.
When traveling to a foreign country, it is important to determine what diseases are common, whether vaccines are needed, and whether they are safe during pregnancy. Human immunodeficiency virus (HIV) infection can be passed from a mother to her baby. The chances of this happening are decreased substantially with certain medication programs during pregnancy. Pregnant women are routinely offered testing for HIV infection. Women with previously undetected infection who are found to have HIV infection can be given special medication to try to protect the baby. At the same time, the medication may benefit the health of the mother herself.

Varicella, or chickenpox, can cause pneumonia or even death in older adults and in pregnant women. Varicella vaccine is available for women who are not immune to chickenpox. Women who had chickenpox in the past do not need a vaccine because they are immune. Women who are not sure if they are immune can receive a blood test to determine immunity status. A vaccine would be given if the blood test showed they were not immune.

What inherited (genetic) diseases can play a role in pregnancy planning?

Certain diseases, such as Tay-Sachs, sickle cell anemia, hemophilia, cystic fibrosis, and certain neurological diseases are genetically inherited. Healthy couples with family histories of these conditions may themselves be carriers of these genetic traits. Blood tests can be performed to screen for certain genetic traits prior to conceiving. Genetic counseling is given to couples who may carry genetic diseases as part of pregnancy planning.
Older women have an increased risk of having babies with chromosome abnormalities, leading to cognitive disabilities and other birth defects. Chromosomal abnormalities (like Downs syndrome ) can lead to birth defects and cognitive disabilities. Pregnant women older than 35 years may consider amniocentesis to detect these chromosomal abnormalities. During amniocentesis, amniotic fluid samples are aspirated from the womb. Chromosome analysis can be performed on fetal cells within the amniotic fluid.
Phenylketonuria is an inherited disease that affects the utilization of a certain protein component in foods. This disorder can be detected by a blood test. Mothers with phenylketonuria may give birth to developmentally disabled children unless their diets are strictly controlled to exclude phenylalanine.

Can I travel by air during pregnancy?

The American College of Obstetrics and Gynecology guidelines say that air travel is safe for most pregnant women up to 36 weeks gestation, as long as there are no obstetric or maternal complications already diagnosed. Examples of special situations would be women with hypertension, poorly-controlled diabetes, or sickle cell disease, or women diagnosed with increased risk of premature labor. Support stockings during flight, and intermittent walking to move the legs around are recommended to minimize the chance of blood clots in the legs during prolonged flights. Travel plans should be discussed with the monitoring health care professional in high-risk pregnancies.

Can I have intercourse during pregnancy?

Intercourse during pregnancy is safe for most women. Special situations in which women might be advised to avoid intercourse include prior preterm labor, multiple miscarriages, infection, bleeding, amniotic fluid leak, and a condition called placenta previa or low placenta. (A placenta previa is when the placenta is implanted near the outlet of the uterus, so that at the time of delivery the placenta precedes the baby. Placenta previa can cause painless bleeding in the last trimester of pregnancy, and may be a reason for a C-section.)
All women are advised to avoid sexual intercourse that could put them at risk to exposure to sexually transmitted diseases.

How soon after stopping birth control can I become pregnant?

There is no evidence that there is increased risk of spontaneous abortion increases if a woman becomes pregnant in the first cycles after stopping oral contraceptive pills. Intrauterine devices (IUD's) are not harmful to the fetus. Women who get pregnant with an IUD that is still in place do not have higher change of congenital abnormalities in the fetus compared to other women. If the IUD of a woman in her 1st trimester is carefully removed by a doctor, or if it is expelled on its own in the 1st trimester, the chance of spontaneous miscarriage is not increased compared to other women.
When barrier methods such as condoms, diaphragms, cervical caps, and sponges are used, pregnancy can occur by simply discontinuing their use during a regular cycle. The same can be said for spermicidal gels and suppositories.
Medroxyprogesterone (Depo-Provera) is an injectable hormone used for contraception. The contraceptive effect of Depo-Provera may last as long as 18 months after the last injection. Normal menstrual cycles and pregnancy cannot occur until after the contraceptive effect wears off.

How do we maximize our chances of becoming pregnant?

For most couples, becoming pregnant occurs naturally. Some couples have difficulty conceiving, and ways to maximize chances of conception become important. Other parents may want to time the delivery of their babies during particular times of the year or space the birth of their babies according to a desired schedule.
The first step in maximizing the chances of conception is by estimating the time of ovulation. Ovulation is that time of the menstrual cycle wherein the egg is released from the ovary and travels towards the Fallopian tube. In women with regular menstrual cycles, ovulation usually occurs 12-14 days prior to the onset of the next menstrual flow. Simply counting back fourteen days from the expected date of the onset of next period should be the time of ovulation. The couple should have intercourse for several days before, day of, and day after the expected time of ovulation. There is usually some variation in the time of ovulation even in women with regular cycles, so a few extra days of intercourse before and after expected ovulation is advised.
If the cycles are irregular and unpredictable, estimating the time of ovulation becomes difficult, and professional assistance may be helpful. Another option for a woman with irregular cycles is the use of ovulation predictor kits available over-the-counter at most drug and grocery stores. These kits can be used to determine the approximate time of ovulation by detecting urinary hormone elevations that precede ovulation. Another approach is to have intercourse every other day throughout the menstrual cycle. This approach will take out the stress or anxiety involved in timing intercourse.
Basal body temperature timing is a technique of checking the body temperature every morning and charting the results. If the temperature rises by a certain amount and stays elevated, it can be assumed that ovulation occurred. Difficulties with this method are that it is tedious and only provides the woman with information about ovulation after it has occurred.
Ultrasound images of the ovaries can be performed to monitor the growth and collapse of the ovarian follicle during the cycle. The follicle is the fluid-filled structure that surrounds the egg, and it can easily be seen on ultrasound. This method is probably the most accurate in timing ovulation. It is also the most expensive and is usually reserved for selected couples who are experiencing difficulty in becoming pregnant.
It is important to remember that even though intercourse and ovulation coincide, pregnancy may still not be achieved in any given menstrual cycle or even after several consecutive menstrual cycles. In many situations, the failure to conceive after multiple attempts is not a reason for alarm. It is not uncommon for pregnancy to occur only after several months of consistent attempts. Couples who have experienced an inability to conceive after several cycles may consider seeking professional advice to determine if an infertility evaluation is necessary.

Can I do something to help my chances of conceiving a boy or a girl?

The ancient Greeks tied off the left testicle when attempting to conceive a boy.
French noblemen in the 18th century went one step further and actually removed the left testicle, believing that this would guarantee a male infant.
In the 19th century, the man would stand on the right bedpost and the woman would lie on her right side after intercourse in order to assure a boy!
The 20th century brought on the ideas of deep penetration, adjustment of vaginal acidity, consumption of certain foods, position, and other various methods to enhance the chances of bearing either a girl or a boy.

None of these various approaches has ever been scientifically tested. Therefore, no definite statement can be given regarding the success of these techniques, but they probably have no impact on the gender of the baby. Currently there have been a few proven laboratory techniques of increasing the percentage of male or female sperm, but these are not routinely used. These techniques either use electrical charges, or special "gels" through which the sperm have to swim. Even with these techniques, there is no guarantee that a child of the desired gender will be born. Research has refuted any relationship between the timing of sexual intercourse in relation to ovulation and the gender of the baby.

REFERENCES:
eMedicine.com. Pregnancy Diagnosis.

eMedicine.com. Common Pregnancy Complaints and Questions.

Previous contributing authors: Leon J. Baginski, MD, FACOG and Carolyn Janet Crandall, MD

Source:Medicinenet.com.

Medical Author:

Melissa Conrad Stöppler, MD

Medical Editor:

William C. Shiel Jr., MD, FACP, FACR

Systemic Lupus Erythematosus (SLE or Lupus)

2012-03-17T04:21:00.001-07:00

What is lupus? What are the types of lupus?

Lupus is an autoimmune disease characterized by acute and chronic inflammation of various tissues of the body. Autoimmune diseases are illnesses that occur when the body's tissues are attacked by its own immune system. The immune system is a complex system within the body that is designed to fight infectious agents, such as bacteria and other foreign microbes. One of the ways that the immune system fights infections is by producing antibodies that bind to the microbes. People with lupus produce abnormal antibodies in their blood that target tissues within their own body rather than foreign infectious agents. Because the antibodies and accompanying cells of inflammation can affect tissues anywhere in the body, lupus has the potential to affect a variety of areas. Sometimes lupus can cause disease of the skin, heart, lungs, kidneys, joints, and/or nervous system. When only the skin is involved, the condition is called lupus dermatitis or cutaneous lupus erythematosus. A form of lupus dermatitis that can be isolated to the skin, without internal disease, is called discoid lupus. When internal organs are involved, the condition is referred to as systemic lupus erythematosus (SLE).
Both discoid and systemic lupus are more common in women than men (about eight times more common). The disease can affect all ages but most commonly begins from 20-45 years of age. Statistics demonstrate that lupus is somewhat more frequent in African Americans and people of Chinese and Japanese descent.

What causes lupus? Is lupus hereditary?

The precise reason for the abnormal autoimmunity that causes lupus is not known. Inherited genes, viruses, ultraviolet light, and certain medications may all play some role.
Genetic factors increase the tendency of developing autoimmune diseases, and autoimmune diseases such as lupus, rheumatoid arthritis, and autoimmune thyroid disorders are more common among relatives of people with lupus than the general population. Some scientists believe that the immune system in lupus is more easily stimulated by external factors like viruses or ultraviolet light. Sometimes, symptoms of lupus can be precipitated or aggravated by only a brief period of sun exposure.
It also is known that some women with SLE can experience worsening of their symptoms prior to their menstrual periods. This phenomenon, together with the female predominance of SLE, suggests that female hormones play an important role in the expression of SLE. This hormonal relationship is an active area of ongoing study by scientists.
More recently, research has demonstrated evidence that a key enzyme's failure to dispose of dying cells may contribute the development of SLE. The enzyme, DNase1, normally eliminates what is called "garbage DNA" and other cellular debris by chopping them into tiny fragments for easier disposal. Researchers turned off the DNase1 gene in mice. The mice appeared healthy at birth, but after six to eight months, the majority of mice without DNase1 showed signs of SLE. Thus, a genetic mutation in a gene that could disrupt the body's cellular waste disposal may be involved in the initiation of SLE.

What is drug-induced lupus?

Dozens of medications have been reported to trigger SLE. However, more than 90% of cases of "drug-induced lupus" occurs as a side effect of one of the following six drugs: hydralazine (Apresoline is used for high blood pressure); quinidine (Quinidine Gluconate, Quinidine Sulfate) and procainamide (Pronestyl; Procan-SR; Procanbid) are used for abnormal heart rhythms; phenytoin (Dilantin) is used for epilepsy; isoniazid ([Nydrazid, Laniazid] used for tuberculosis); and d-penicillamine (used for rheumatoid arthritis). These drugs are known to stimulate the immune system and cause SLE. Fortunately, drug-induced SLE is infrequent (accounting for less than 5% of all people with SLE) and usually resolves when the medications are discontinued.

What are lupus symptoms and signs?

People with SLE can develop different combinations of symptoms and organ involvement. Common complaints and symptoms include fatigue, low-grade fever, loss of appetite, muscle aches, arthritis, ulcers of the mouth and nose, facial rash ("butterfly rash"), unusual sensitivity to sunlight (photosensitivity), inflammation of the lining that surrounds the lungs (pleuritis) and the heart (pericarditis), and poor circulation to the fingers and toes with cold exposure (Raynaud's phenomenon). Complications of organ involvement can lead to further symptoms that depend on the organ affected and severity of the disease.
Skin manifestations are frequent in lupus and can sometimes lead to scarring. In discoid lupus, only the skin is typically involved. The skin rash in discoid lupus often is found on the face and scalp. It usually is red and may have raised borders. Discoid lupus rashes are usually painless and do not itch, but scarring can cause permanent hair loss (alopecia). Over time, 5%-10% of those with discoid lupus may develop SLE.
Over half of the people with SLE develop a characteristic red, flat facial rash over the bridge of their nose. Because of its shape, it is frequently referred to as the "butterfly rash" of SLE. The rash is painless and does not itch. The facial rash, along with inflammation in other organs, can be precipitated or worsened by exposure to sunlight, a condition called photosensitivity. This photosensitivity can be accompanied by worsening of inflammation throughout the body, called a "flare" of the disease.

Picture of a butterfly rash on the face, a characteristic sign of systemic lupus erythematosus (SLE)

Typically, with treatment, this rash can heal without permanent scarring.
Most people with SLE will develop arthritis during the course of their illness. Arthritis in SLE commonly involves swelling, pain, stiffness, and even deformity of the small joints of the hands, wrists, and feet. Sometimes, the arthritis of SLE can mimic that of rheumatoid arthritis (another autoimmune disease).
More serious organ involvement with inflammation occurs in the brain, liver, and kidneys. White blood cells and blood-clotting factors also can be characteristically decreased in SLE, known as leukopenia (leucopenia) and thrombocytopenia, respectively. Leukopenia can increase the risk of infection, and thrombocytopenia can increase the risk of bleeding.
Inflammation of muscles (myositis) can cause muscle pain and weakness. This can lead to elevations of muscle enzyme levels in the blood.
Inflammation of blood vessels (vasculitis) that supply oxygen to tissues can cause isolated injury to a nerve, the skin, or an internal organ. The blood vessels are composed of arteries that pass oxygen-rich blood to the tissues of the body and veins that return oxygen-depleted blood from the tissues to the lungs. Vasculitis is characterized by inflammation with damage to the walls of various blood vessels. The damage blocks the circulation of blood through the vessels and can cause injury to the tissues that are supplied with oxygen by these vessels.
Inflammation of the lining of the lungs (pleuritis) and of the heart (pericarditis) can cause sharp chest pain. The chest pain is aggravated by coughing, deep breathing, and certain changes in body position. The heart muscle itself rarely can become inflamed (carditis). It has also been shown that young women with SLE have a significantly increased risk of heart attacks due to coronary artery disease.
Kidney inflammation in SLE can cause leakage of protein into the urine, fluid retention, high blood pressure, and even kidney failure. This can lead to further fatigue and swelling of the legs and feet. With kidney failure, machines are needed to cleanse the blood of accumulated waste products in a process called dialysis.
Involvement of the brain can cause personality changes, thought disorders (psychosis), seizures, and even coma. Damage to nerves can cause numbness, tingling, and weakness of the involved body parts or extremities. Brain involvement is referred to as lupus cerebritis.
Many people with SLE experience hair loss (alopecia). Often, this occurs simultaneously with an increase in the activity of their disease. The hair loss can be patchy or diffuse and appear to be more like hair thinning.
Some people with SLE have Raynaud's phenomenon. In this condition, the blood supply to the fingers and/or toes becomes compromised upon exposure to cold, causing blanching, whitish and/or bluish discoloration, and pain and numbness in the exposed fingers and toes.
Other conditions that can accompany lupus include fibromyalgia, coronary heart disease, nonbacterial valvular heart disease, pancreatitis, esophagus disease with difficulty swallowing (dysphagia), liver disease (lupoid hepatitis), and infections.

How is lupus diagnosed?

Since individuals with SLE can have a wide variety of symptoms and different combinations of organ involvement, no single test establishes the diagnosis of systemic lupus. To help doctors improve the accuracy of the diagnosis of SLE, 11 criteria were established by the American Rheumatism Association. These 11 criteria are closely related to the symptoms discussed above. Some people suspected of having SLE may never develop enough criteria for a definite diagnosis. Other people accumulate enough criteria only after months or years of observation. When a person has four or more of these criteria, the diagnosis of SLE is strongly suggested. Nevertheless, the diagnosis of SLE may be made in some settings in people with only a few of these classical criteria, and treatment may sometimes be instituted at this stage. Of these people with minimal criteria, some may later develop other criteria, but many never do.
The 11 criteria used for diagnosing systemic lupus erythematosus are

malar (over the cheeks of the face) "butterfly" rash,
discoid skin rash (patchy redness with hyperpigmentation and hypopigmentation that can cause scarring),
photosensitivity (skin rash in reaction to sunlight [ultraviolet light] exposure),
mucous membrane ulcers (spontaneous ulcers of the lining of the mouth, nose, or throat),
arthritis (two or more swollen, tender joints of the extremities),
pleuritis or pericarditis (inflammation of the lining tissue around the heart or lungs, usually associated with chest pain upon breathing or changes of body position),
kidney abnormalities (abnormal amounts of urine protein or clumps of cellular elements called casts detectable with a urinalysis),
brain irritation (manifested by seizures [convulsions] and/or psychosis),
blood-count abnormalities (low counts of white or red blood cells, or platelets, on routine blood testing),
immunologic disorder (abnormal immune tests include anti-DNA or anti-Sm [Smith] antibodies, falsely positive blood test for syphilis, anticardiolipin antibodies, lupus anticoagulant, or positive LE prep test),
and antinuclear antibody (positive ANA antibody testing [antinuclear antibodies in the blood]).

In addition to the 11 criteria, other tests can be helpful in evaluating people with SLE to determine the severity of organ involvement. These include routine testing of the blood to detect inflammation (for example, tests called the sedimentation rate and C-reactive protein), blood-chemistry testing, direct analysis of internal body fluids, and tissue biopsies. Abnormalities in body fluids and tissue samples (kidney, skin, and nerve biopsies) can further support the diagnosis of SLE. The appropriate testing procedures are selected for the patient individually by the doctor.

What is the treatment for systemic lupus erythematosus?

There is no permanent cure for SLE. The goal of treatment is to relieve symptoms and protect organs by decreasing inflammation and/or the level of autoimmune activity in the body. The precise treatment is decided on an individual basis. Many people with mild symptoms may need no treatment or only intermittent courses of anti-inflammatory medications. Those with more serious illness involving damage to internal organ(s) may require high doses of corticosteroids in combination with other medications that suppress the body's immune system.
People with SLE need more rest during periods of active disease. Researchers have reported that poor sleep quality was a significant factor in developing fatigue in people with SLE. These reports emphasize the importance for people and physicians to address sleep quality and the effect of underlying depression, lack of exercise, and self-care coping strategies on overall health. During these periods, carefully prescribed exercise is still important to maintain muscle tone and range of motion in the joints.
Nonsteroidal anti-inflammatory drugs (NSAIDs) are helpful in reducing inflammation and pain in muscles, joints, and other tissues. Examples of NSAIDs include aspirin, ibuprofen (Motrin), naproxen (Naprosyn), and sulindac (Clinoril). Since the individual response to NSAIDs varies, it is common for a doctor to try different NSAIDs to find the most effective one with the fewest side effects. The most common side effects are stomach upset, abdominal pain, ulcers, and even ulcer bleeding. NSAIDs are usually taken with food to reduce side effects. Sometimes, medications that prevent ulcers while taking NSAIDs, such as misoprostol (Cytotec), are given simultaneously.
Corticosteroids are more potent than NSAIDs in reducing inflammation and restoring function when the disease is active. Corticosteroids are particularly helpful when internal organs are affected. Corticosteroids can be given by mouth, injected directly into the joints and other tissues, or administered intravenously. Unfortunately, corticosteroids have serious side effects when given in high doses over prolonged periods, and the doctor will try to monitor the activity of the disease in order to use the lowest doses that are safe. Side effects of corticosteroids include weight gain, thinning of the bones and skin, infection, diabetes, facial puffiness, cataracts, and death (necrosis) of the tissues in large joints.
Hydroxychloroquine (Plaquenil) is an antimalarial medication found to be particularly effective for SLE people with fatigue, skin involvement, and joint disease. Consistently taking Plaquenil can prevent flare-ups of lupus. Side effects are uncommon but include diarrhea, upset stomach, and eye-pigment changes. Eye-pigment changes are rare but require monitoring by an ophthalmologist (eye specialist) during treatment with Plaquenil. Researchers have found that Plaquenil significantly decreased the frequency of abnormal blood clots in people with systemic lupus. Moreover, the effect seemed independent of immune suppression, implying that Plaquenil can directly act to prevent the blood clots. This fascinating study highlights an important reason for people and doctors to consider Plaquenil for long-term use, especially for those SLE people who are at some risk for blood clots in veins and arteries, such as those with phospholipid antibodies (cardiolipin antibodies, lupus anticoagulant, and false-positive venereal disease research laboratory test). This means not only that Plaquenil reduces the chance for re-flares of SLE, but it can also be beneficial in thinning the blood to prevent abnormal excessive blood clotting. Plaquenil is commonly used in combination with other treatments for lupus.
For resistant skin disease, other antimalarial drugs, such as chloroquine (Aralen) or quinacrine, are considered and can be used in combination with hydroxychloroquine. Alternative medications for skin disease include dapsone and retinoic acid (Retin-A). Retin-A is often effective for an uncommon wart-like form of lupus skin disease. For more severe skin disease, immunosuppressive medications are considered as described below.
Medications that suppress immunity (immunosuppressive medications) are also called cytotoxic drugs. Immunosuppressive medications are used for treating people with more severe manifestations of SLE, such as damage to internal organ(s). Examples of immunosuppressive medications include methotrexate (Rheumatrex, Trexall), azathioprine (Imuran), cyclophosphamide (Cytoxan), chlorambucil (Leukeran), and cyclosporine (Sandimmune). All immunosuppressive medications can seriously depress blood-cell counts and increase risks of infection and bleeding. Immunosuppressive medications may not be taken during pregnancy or conception because of risk to the fetus. Other side effects are specific for each drug. For examples, Rheumatrex can cause liver toxicity, while Sandimmune can impair kidney function.
In recent years, mycophenolate mofetil (CellCept) has been used as an effective medication for lupus, particularly when it is associated with kidney disease. CellCept has been helpful in reversing active lupus kidney disease (lupus renal disease) and in maintaining remission after it is established. Its lower side-effect profile has advantage over traditional immune-suppression medications.
In SLE patients with serious brain or kidney disease, plasmapheresis (a process of removing and treating the blood before it is returned to the body) is sometimes used to remove antibodies and other immune substances from the blood to suppress immunity. Rarely, people with SLE can develop seriously low platelet levels, thereby increasing the risk of excessive and spontaneous bleeding. Since the spleen is believed to be the major site of platelet destruction, surgical removal of the spleen is sometimes performed to improve platelet levels. Other treatments have included plasmapheresis and the use of male hormones. Plasmapheresis has also been used to remove proteins (cryoglobulins) that can lead to vasculitis. End-stage kidney damage from SLE requires dialysis and/or a kidney transplant.
Most recent research is indicating benefits of rituximab (Rituxan) in treating lupus. Rituximab is an intravenously infused antibody that suppresses a particular white blood cell, the B cell, by decreasing their number in the circulation. B cells have been found to play a central role in lupus activity, and when they are suppressed, the disease tends toward remission. This may particularly helpful for people with kidney disease.
Another new B-cell-suppressing treatment is belimumab (Benlysta). Belimumab blocks the stimulation of the B cells (a B-lymphocyte stimulator or BLyS-specific inhibitor) and is indicated for the treatment of adult patients with active, autoantibody-positive systemic lupus erythematosus who are receiving standard therapy. It is important to note that the efficacy of belimumab has not been evaluated in patients with severe active lupus nephritis or severe active central nervous system lupus. Belimumab has not been studied in combination with other biologic therapies or intravenous cyclophosphamide.
Scientists have also found that low-dose dietary supplementation with omega-3 fish oils could help patients with lupus by decreasing disease activity and possibly decreasing heart-disease risk.

How can a lupus patient help prevent disease activity (flares)?

SLE is undoubtedly a potentially serious illness with involvement of numerous organ systems. However, it is important to recognize that most people with SLE lead full, active, and healthy lives. Periodic increases in disease activity (flares) can usually be managed by varying medications. Since ultraviolet light can precipitate and worsen flares, people with systemic lupus should avoid sun exposure. Sunscreens and clothing covering the extremities can be helpful. Abruptly stopping medications, especially corticosteroids, can also cause flares and should be avoided. People with SLE are at increased risk of infections, especially if they are taking corticosteroids or immunosuppressive medications. Therefore, any unexpected fever should be reported and evaluated.
The key to successful management of SLE is regular contact and communication with the doctor, allowing monitoring of symptoms, disease activities, and treatment of side effects.

How can systemic lupus erythematosus affect pregnancy or the newborn?

Women with SLE who become pregnant are considered "high risk." Women with SLE who are pregnant require close observation during pregnancy, delivery, and the postpartum period. This includes fetal monitoring by the obstetrician during later pregnancy. These women can have an increased risk of miscarriages (spontaneous abortions) and can have flares of SLE during pregnancy. The presence of phospholipid antibodies, such as cardiolipin antibodies or lupus anticoagulant, in the blood can identify people at risk for miscarriages. Cardiolipin antibodies are associated with a tendency toward blood clotting. People with SLE who have cardiolipin antibodies or lupus anticoagulant may need blood-thinning medications (aspirin with or without heparin) during pregnancy to prevent miscarriages. Other reported treatments include the use of intravenous gamma globulin for selected people with histories of premature miscarriage and those with low blood-clotting elements (platelets) during pregnancy. Pregnant women who have had a previous blood-clotting event may benefit by continuation of blood-thinning medications throughout and after pregnancy for up to six to 12 weeks, at which time the risk of clotting associated with pregnancy seems to diminish. Plaquenil has now been found to be safe for use to treat SLE during pregnancy.
Lupus antibodies can be transferred from the mother to the fetus and result in lupus illness in the newborn ("neonatal lupus"). This includes the development of low red cell (anemia) and/or white blood cell and platelet counts and skin rash. Problems can also develop in the electrical system of the baby's heart (congenital heart block). Occasionally, a pacemaker for the baby's heart is needed in this setting. Neonatal lupus and congenital heart block are more common in newborns of mothers with SLE who carry antibodies referred to as anti-Ro (or SS-A) and anti-La (or SS-B). (It is wise for the newborn baby's doctor to be made aware if the mother is known to carry these antibodies, even prior to delivery. The risk of heart block is 2%; the risk of neonatal lupus is 5%.) Neonatal lupus usually clears after 6 months of age, as the mother's antibodies are slowly metabolized by the baby.

What does the future hold for people with lupus?

Overall, the outlook for people with systemic lupus is improving each decade with the development of more accurate monitoring tests and treatments.
The role of the immune system in causing diseases is becoming better understood through research. This knowledge will be applied to design safer and more effective treatment methods. For example, completely revising the immune system of people with extremely aggressive treatments that virtually temporarily wipe out the immune system is being evaluated. Current studies involve immune eradication with or without replacement of cells that can re-establish the immune system (stem cell transplantation).
It should be noted that people with SLE are at a somewhat increased risk for developing cancer. The cancer risk is most dramatic for blood cancers, such as leukemia and lymphoma, but is also increased for breast cancer. This risk probably relates, in part, to the altered immune system that is characteristic of SLE.
Women with SLE appear to be at increased risk for heart disease (coronary artery disease) according to recent reports. Women with SLE should be evaluated and counseled to minimize risk factors for heart disease, such as elevated blood cholesterol, quitting smoking, high blood pressure, and obesity.
DHEA (dehydroepiandrosterone) has been helpful in reducing fatigue, improving thinking difficulties, and improving quality of life in people with SLE. Recent research indicates that DHEA has been shown to improve or stabilize signs and symptoms of SLE. DHEA is commonly available in health-food stores, pharmacies, and many groceries.
Landmark research has shown clearly that oral contraceptives do not increase the rate of flares of systemic lupus erythematosus. This important finding is opposite to what has been thought for years. Now we can reassure women with lupus that if they take birth-control pills, they are not increasing their risk for lupus flares. NOTE: Birth-control pills or any estrogen medications should still be avoided by women who are at increased risk of blood clotting, such as women with lupus who have phospholipid antibodies (including cardiolipin antibody and lupus anticoagulant).
Individuals with SLE can improve their prognosis by learning about the many aspects of the illness as well as closely monitoring their own health with their doctors.

Where can one get more information about lupus?

For more information about systemic lupus erythematosus, see the following sites:
The Arthritis Foundation (http://www.arthritis.org)
PO Box 19000
Atlanta, GA 30326
Lupus Foundation of Minnesota (http://www.lupusmn.org)

Systemic Lupus Erythematosus At A Glance

Systemic lupus erythematosus (SLE) is an autoimmune disease.
SLE is characterized by the production of unusual antibodies in the blood.
SLE is eight times more common in women than men.
The cause(s) of SLE is (are) unknown, however, heredity, viruses, ultraviolet light, and drugs all may play some role.
Up to 10% of people with lupus isolated to the skin will develop the systemic form of lupus (SLE).
Eleven criteria help doctors to diagnose SLE.
Treatment of SLE is directed toward decreasing inflammation and/or the level of autoimmune activity.
People with SLE can prevent "flares" of disease by avoiding sun exposure and not abruptly discontinuing medications and monitoring their condition with their doctor.

REFERENCE:

Harris, Edward, et al. Kelley's Textbook of Rheumatology. Philadelphia: Saunders, 2008.

Medical Author:

William C. Shiel Jr., MD, FACP, FACR

Medical Editor:

Melissa Conrad Stöppler, MD

Source:Medicinenet.com.

Edema

2012-03-17T04:19:00.001-07:00

What is edema?

Edema is observable swelling from fluid accumulation in body tissues. Edema most commonly occurs in the feet and legs, where it is referred to as peripheral edema. The swelling is the result of the accumulation of excess fluid under the skin in the spaces within the tissues. All tissues of the body are made up of cells and connective tissues that hold the cells together. This connective tissue around the cells and blood vessels is known as the interstitium. Most of the body's fluids that are found outside of the cells are normally stored in two spaces; the blood vessels (as the "liquid" or serum portion of your blood) and the interstitial spaces (not within the cells). In various diseases, excess fluid can accumulate in either one or both of these compartments.
The body's organs have interstitial spaces where fluid can accumulate. An accumulation of fluid in the interstitial air spaces (alveoli) in the lungs occurs in a disorder called pulmonary edema. In addition, excess fluid sometimes collects in what is called the third space, which includes cavities in the abdomen (abdominal or peritoneal cavity - called "ascites") or in the chest (lung or pleural cavity - called "pleural effusion"). Anasarca refers to the severe, widespread accumulation of fluid in the all of the tissues and cavities of the body at the same time.

What is pitting edema and how does it differ from non-pitting edema?

Pitting edema can be demonstrated by applying pressure to the swollen area by depressing the skin with a finger. If the pressing causes an indentation that persists for some time after the release of the pressure, the edema is referred to as pitting edema. Any form of pressure, such as from the elastic in socks, can induce pitting with this type of edema.
In non-pitting edema, which usually affects the legs or arms, pressure that is applied to the skin does not result in a persistent indentation. Non-pitting edema can occur in certain disorders of the lymphatic system such as lymphedema, which is a disturbance of the lymphatic circulation that may occur after a mastectomy, lymph node surgery, or congenitally. Another cause of non-pitting edema of the legs is called pretibial myxedema, which is a swelling over the shin that occurs in some patients with hyperthyroidism. Non-pitting edema of the legs is difficult to treat. Diuretic medications are generally not effective, although elevation of the legs periodically during the day and compressive devices may reduce the swelling.
The focus of the rest of this article is on pitting edema, as it is by far the most common form of edema.

What causes pitting edema?

Edema is caused by either systemic diseases, that is, diseases that affect the various organ systems of the body, or by local conditions involving just the affected extremities. The most common systemic diseases associated with edema involve the heart, liver, and kidneys. In these diseases, edema occurs primarily because of the body's retention of too much salt (sodium chloride). The excess salt causes the body to retain water. This water then leaks into the interstitial tissue spaces, where it appears as edema.
The most common local conditions that cause edema are varicose veins and thrombophlebitis (inflammation of the veins) of the deep veins of the legs. These conditions can cause inadequate pumping of the blood by the veins (venous insufficiency). The resulting increased back-pressure in the veins forces fluid stay in the extremities (especially the ankles and feet). The excess fluid then leaks into the interstitial tissue spaces, causing edema.

How does salt intake affect edema?

The body's balance of salt is usually well-regulated. A normal person can consume small or large quantities of salt in the diet without concern for developing salt depletion or retention. The intake of salt is determined by dietary patterns and the removal of salt from the body is accomplished by the kidneys. The kidneys have a great capacity to control the amount of salt in the body by changing the amount of salt eliminated (excreted) in the urine. The amount of salt excreted by the kidneys is regulated by hormonal and physical factors that signal whether retention or removal of salt by the kidneys is necessary.
If the blood flow to the kidneys is decreased by an underlying condition such as heart failure, the kidneys react by retaining salt. This salt retention occurs because the kidneys perceive that the body needs more fluid to compensate for the decreased blood flow. If the patient has a kidney disease that impairs the function of the kidneys, the ability to excrete salt in the urine is limited. In both conditions, the amount of salt in the body increases, which causes the patient to retain water and develop edema.
Patients experiencing a disturbance in their ability to normally excrete salt may need to either be placed on a diet limited in salt and/or given diuretic medications (water pills). In the past, patients with diseases associated with edema were placed on diets very restricted in salt intake. With the development of new and very potent diuretic agents, this marked restriction in dietary salt intake is generally no longer necessary. These diuretics work by blocking the reabsorption and retention of salt by the kidneys, thereby increasing the amount of salt and water that is eliminated in the urine.

Why does a patient with heart disease retain fluid?

Heart failure is the result of poor cardiac function and is reflected by a decreased volume of blood pumped out by the heart, called cardiac output. Heart failure can be caused by weakness of the heart muscle, which pumps blood out through the arteries to the entire body, or by dysfunction of the heart valves, which regulate the flow of blood between the chambers of the heart. The diminished volume of blood pumped out by the heart (decreased cardiac output) is responsible for a decreased flow of blood to the kidneys. As a result, the kidneys sense that there is a reduction of the blood volume in the body. To counter the seeming loss of fluid, the kidneys retain salt and water. In this instance, the kidneys are fooled into thinking that the body needs to retain more fluid volume when, in fact, the body already is holding too much fluid.
This fluid increase ultimately results in the buildup of fluid within the lungs, which causes shortness of breath. Because of the decreased volume of blood pumped out by the heart (decreased cardiac output), the volume of blood in the arteries is also decreased, despite the actual increase in the body's total fluid volume. An associated increase in the amount of fluid in the blood vessels of the lungs causes shortness of breath because the excess fluid from the lungs' blood vessels leaks into the airspaces (alveoli) and interstitium in the lungs. This accumulation of fluid in the lung is called pulmonary edema. At the same time, accumulation of fluid in the legs causes pitting edema. This edema occurs because the build-up of blood in the veins of the legs causes leakage of fluid from the legs' capillaries (tiny blood vessels) into the interstitial spaces.
An understanding of how the heart and lungs interact will help you to better comprehend how fluid retention works in heart failure. The heart has four chambers; an auricle and a ventricle on the left side of the heart and an auricle and ventricle on the right. The left auricle receives oxygenated blood from the lungs and transfers it to the left ventricle, which then pumps it through the arteries to the entire body. The blood then is transported back to the heart by veins into the right auricle and transferred to the right ventricle, which then pumps it to the lungs for re-oxygenation.
Left-sided heart failure, which is due primarily to a weak left ventricle, usually is caused by coronary artery disease, hypertension, or disease of the heart valves. Typically, when these patients initially come to the doctor they are troubled by shortness of breath with exertion and when lying down at night (orthopnea). These symptoms are due to pulmonary edema that is caused by pooling of the blood in the vessels of the lungs.
In contrast, right-sided heart failure, which often is due to chronic lung diseases such as emphysema, initially causes salt retention and edema. Persistent salt retention in these patients, however, may lead to an expanded blood volume in the blood vessels, thereby causing fluid accumulation in the lungs (pulmonary congestion) and shortness of breath.
In patients with heart failure due to weak heart muscle (cardiomyopathy), both the right and left ventricles of the heart are usually affected. These patients, therefore, can initially suffer from swelling both in the lungs (pulmonary edema) and in the legs and feet (peripheral edema). The physician examining a patient who has congestive heart failure with fluid retention looks for certain signs. These include:

pitting edema of the legs and feet,
rales in the lungs (moist crackle sounds from the excess fluid that can be heard with a stethoscope),
a gallop rhythm (three heart sounds instead of the normal two due to muscle weakness), and
distended neck veins. The distended neck veins reflect the accumulation of blood in the veins that are returning blood to the heart.

Why do patients with liver disease develop ascites and edema?

In patients with chronic diseases of the liver, fibrosis (scarring) of the liver often occurs. When the scarring becomes advanced, the condition is called cirrhosis of the liver. Ascites is excessive fluid that accumulates in the abdominal (peritoneal) cavity. It is a complication of cirrhosis and appears as an abdominal bulge. The peritoneum is the inner lining of the abdominal cavity, which also folds over to cover the organs inside the abdomen such as the liver, gallbladder, spleen, pancreas, and intestines. Ascites develops because of a combination of two factors:

increased pressure in the vein system that carries blood from the stomach, intestines, and spleen to the liver (portal hypertension); and
a low level of the protein albumin in the blood (hypoalbuminemia). Albumin, which is the predominant protein in the blood and which helps maintain blood volume, is reduced in cirrhosis primarily because the damaged liver is not able to produce enough of it.

Other consequences of portal hypertension include dilated veins in the esophagus (varices), prominent veins on the abdomen, and an enlarged spleen. Each of these conditions is due primarily to the increased pressure and accumulation of blood and excess fluid in the abdominal blood vessels. The fluid of ascites can be removed from the abdominal cavity by using a syringe and a long needle, a procedure called paracentesis. Analysis of the fluid can help differentiate ascites that is caused by cirrhosis from other causes of ascites, such as cancer, tuberculosis, congestive heart failure, and nephrosis. Sometimes, when ascites does not respond to treatment with diuretics, paracentesis can be used to remove large amounts of the ascitic fluid.
Peripheral edema, which is usually seen as pitting edema of the legs and feet, also occurs in cirrhosis. The edema is a consequence of the hypoalbuminemia and the kidneys retaining salt and water.
The presence or absence of edema in patients with cirrhosis and ascites is an important consideration in the treatment of the ascites. In patients with ascites without edema, diuretics must be given with extra caution. Diuresis (induced increased volume of urine by use of diuretics) that is too aggressive or rapid in these patients can lead to a low blood volume (hypovolemia), which can cause kidney and liver failure. In contrast, when patients who have both edema and ascites undergo diuresis, the edema fluid in the interstitial space serves as somewhat of a buffer against the development of low blood volume. The excess interstitial fluid moves into the blood vessel spaces to rapidly replenish the depleted blood volume.

Why does edema occur in patients with kidney disease?

Edema forms in patients with kidney disease for two reasons:

a heavy loss of protein in the urine, or
impaired kidney (renal) function.

Heavy loss of protein in the urine
In this situation, the patients have normal or fairly normal kidney function. The heavy loss of protein in the urine (over 3.0 grams per day) with its accompanying edema is termed the nephrotic syndrome. Nephrotic syndrome results in a reduction in the concentration of albumin in the blood (hypoalbuminemia). Since albumin helps to maintain blood volume in the blood vessels, a reduction of fluid in the blood vessels occurs. The kidneys then register that there is depletion of blood volume and, therefore, attempt to retain salt. Consequently, fluid moves into the interstitial spaces, thereby causing pitting edema.
The treatment of fluid retention in these patients is to reduce the loss of protein into the urine and to restrict salt in the diet. The loss of protein in the urine may be reduced by the use of ACE inhibitors and angiotensin receptor blockers (ARB's). Both categories of drugs, which ordinarily are used to lower blood pressure, prompt the kidneys to reduce the loss of protein into the urine.
ACE inhibitor drugs include:

enalapril (Vasotec),
quinapril (Accupril),
captopril (Capoten),
benazepril (Lotensin),
trandolapril (Mavik),
lisinopril (Zestril or Prinivil), and
ramipril (Altace).

Angiotensin receptor blockers include:

losartan (Cozaar),
valsartan (Diovan),
candesartan (Atacand), and
irbesartan (Avapro).

Certain kidney diseases may contribute to the loss of protein in the urine and the development of edema. A biopsy of the kidney may be needed to make a diagnosis of the type of kidney disease, so that treatment may be given.
Impaired kidney (renal) function
In this situation, patients who have kidney diseases that impair renal function develop edema because of a limitation in the kidneys' ability to excrete sodium into the urine. Thus, patients with kidney failure from whatever cause will develop edema if their intake of sodium exceeds the ability of their kidneys to excrete the sodium. The more advanced the kidney failure, the greater the problem of salt retention is likely to become. The most severe situation is the patient with end-stage kidney failure who requires dialysis therapy. This patient's salt balance is totally regulated by dialysis, which can remove salt during the treatment. Dialysis is a method of cleansing the body of the impurities that accumulate when the kidneys fail. Dialysis is accomplished by circulating the patient's blood over an artificial membrane (hemodialysis) or by using the patient's own abdominal cavity (peritoneal membrane) as the cleansing surface. Individuals whose kidney function declines to less than 5% to 10% of normal may require dialysis.

What is idiopathic edema?

Idiopathic edema is a pitting edema of unknown cause that occurs primarily in pre-menopausal women who do not have evidence of heart, liver, or kidney disease. In this condition, the fluid retention at first may be seen primarily pre-menstrually (just prior to menstruation), which is why it sometimes is called "cyclical" edema. However, it can become a more constant and severe problem.
Patients with idiopathic edema often take diuretics to decrease the edema in order to lessen the discomfort of bloating and swelling. Paradoxically, however, the edema in this condition can become more of a problem after the use of diuretics. The patients can develop fluid retention as a rebound phenomenon each time they discontinue diuretics. It is important to talk to your doctor before using any diuretics.
Patients with idiopathic edema appear to have a leak in the capillaries (tiny peripheral blood vessels that connect the arteries with the veins) so that fluid passes from the blood vessels into the surrounding interstitial space. Thus, a patient with idiopathic edema has a decreased blood volume, which leads to the typical reaction of salt retention by the kidneys.

The leg edema in these patients is exaggerated in the standing position, since edema tends to accumulate in those parts of the body that are close to the ground at the time.
These patients often have edema around the eyes (periorbital edema) in the morning because the edema fluid accumulates during the night around their eyes as they lay sleeping flat.

In contrast, edema around the eyes does not tend to develop in cardiac patients who keep their heads elevated at night because of shortness of breath when they lie flat. These patients characteristically experience varying amounts of edema in different parts of the body at different times of the day.
Patients with idiopathic edema often become dependant on diuretics, and this dependance is often difficult to interrupt. A period as long as three weeks off diuretics may be required to break the dependency cycle. The withdrawal from diuretics may lead to fluid retention that produces major discomfort and swelling. Furthermore, there are definite risks associated with the prolonged use of diuretics in these individuals, which are compounded by the tendency to increase the doses of the diuretics.
As a result of chronic diuretic use and abuse, patients may develop:

a deficiency of potassium,
depletion of blood volume in the blood vessels, and
kidney insufficiency or failure.

Other side effects of diuretics include:

high blood sugar (diabetes),
high uric acid (gout),
muscle cramps, tender and enlarged breasts (gynecomastia), and
pancreatitis (inflammation of the pancreas).

Although withdrawal from diuretics is the most important factor in treating these patients, other medications have been used to try to minimize the fluid retention. These medications include ACE inhibitors, low-dose amphetamines, ephedrine, bromocriptine (Parlodel), or levodopa-carbidopa (Sinemet) in combination. However, their effectiveness is uncertain and side effects of these drugs may occur. For example, hypotension (low blood pressure) may be seen with the use of ACE inhibitors, especially if the patient is also taking diuretics.

How does venous insufficiency cause edema?

The veins in the legs are responsible for transporting blood up to the veins of the torso, where it is then returned to the heart. The veins of the legs have valves that prevent the backward flow of blood within them. Venous insufficiency is incompetence of the veins that occurs because of dilation, or enlargement, of the veins and dysfunction of their valves. This happens, for example, in patients with varicose veins. Venous insufficiency leads to a backup of blood and increased pressure in the veins, thereby resulting in edema of the legs and feet. Edema of the legs also can occur with an episode of deep vein thrombophlebitis, which is a blood clot within an inflamed vein. In this situation, the clot in the deep vein blocks the return of blood, and consequently causes increased back-pressure in the leg veins.
Venous insufficiency is a problem that is localized to the legs, ankles, and feet. One leg may be more affected than the other (asymmetrical edema). In contrast, systemic diseases that are associated with fluid retention generally cause the same amount of edema in both legs, and can also cause edema and swelling elsewhere in the body. The response to therapy with diuretic drugs in patients with venous insufficiency tends to be unsatisfactory. This is because the continued pooling of fluid in the lower extremities makes it difficult for the diuretics to mobilize the edema fluid. Elevation of the legs periodically during the day and the use of compression stockings may alleviate the edema. Some patients require surgical treatment to relieve chronic edema that is caused by venous insufficiency.

Which diuretics are used to treat edema?

Edema can become a problem in systemic diseases of the heart, liver or kidneys. Diuretic therapy can be initiated, often alleviating the edema. The most potent diuretics are loop diuretics, so-called because they work in the portion of the kidney tubules referred to as the loop of Henle. The kidney tubules are small ducts that regulate salt and water balance, while transporting the forming urine. Clinical loop diuretics available are:

furosemide (Lasix),
torsemide (Demadex), and
butethamine (Bumex).

The doses of these diuretics vary depending upon the clinical circumstances. These drugs can be given orally, although seriously ill patients in the hospital may receive them intravenously for more prompt or effective response. If one of the loop diuretics is not effective alone, it may be combined with an agent that works further down (more distally) in the tubule. These agents include the thiazide type diuretics, such as hydrochlorothiazide (HydroDIURIL), or a similar but more potent type of diuretic called metolazone (Zaroxolyn). When diuretics that work at different sites in the kidney are used together, the response often is greater than the combined responses to the individual diuretics (synergistic response).
Some diuretics frequently cause an excessive loss of potassium in the urine, leading to the depletion of body potassium. These drugs include the loop diuretics, the thiazide diuretics, and metolazone. Patients on these diuretics are commonly advised to take potassium supplements and/or to eat foods high in potassium. High potassium foods include certain fruits such as:

bananas,
orange juice,
tomatoes, and
potatoes.

Patients with impaired kidney function often do not require potassium supplements with diuretics because their damaged kidneys tend to retain potassium. In certain instances, the volume of urine induced by the diuretic can be improved by adding a potassium-sparing diuretic, one that does not cause depletion of potassium. These diuretics include spironolactone (Aldactone), triamterene (Dyrenium, a component of Dyazide), and amiloride (Midamor). Adding one of these diuretics to the patient's diuretic regimen may preclude the need for potassium supplements. Another diuretic that can be used is acetazolamide (Diamox), which counteracts the development of an increased concentration of bicarbonate (too much alkali) in the blood. Increased bicarbonate sometimes occurs in patients receiving other diuretics.

Are diuretics used for other purposes?

Diuretics have several other uses in addition treating edema.

A diuretic may be used as part of the treatment program for patients with hypertension. (High blood pressure may be caused by salt retention, or caused by some antihypertensive medications). In fact, most medications that dilate the blood vessels and reduce blood pressure, except for ACE inhibitors and angiotensin receptor blockers, lead to secondary salt retention by the kidneys.
Thiazide diuretics also have been used to prevent the formation of kidney stones. These drugs reduce the urinary excretion of calcium, which is a component of the kidney stone.
Acetazolamide (Diamox) taken a few days before going to high altitudes, appears to reduce the tendency for people to develop altitude sickness.

Edema At A Glance

Edema is a swelling, usually of the legs, due to the accumulation of excessive fluid in the tissues.
The edema that occurs in diseases of the heart, liver, and kidneys is mainly caused by salt retention, which holds the excess fluid in the body.
In certain liver and kidney diseases, low levels of albumin in the blood can contribute to fluid retention.
Heart failure, cirrhosis of the liver, and a kidney disease called nephrotic syndrome are the most common systemic diseases that cause edema.
Excess fluid that accumulates in the lungs is called pulmonary edema.
Excess fluid that accumulates in the abdominal cavity is called ascites.
Edema of unknown cause occurs primarily in women.
Varicose veins or thrombophlebitis (a blood clot in an inflamed vein) of the deep veins in the legs causes edema that is localized to the legs.
Therapy for edema consists of treating the underlying conditions, restricting salt intake, and often using diuretics (medicines to induce urination).

Reference: Harrison's Principles of Internal Medicine, McGraw-Hill, edited by Eugene Braunwald, et. al., 2001

Previous contributing authors and editors:

Medical Author: Mark Scott Noah, MD
Medical Editor: Leslie J. Schoenfield, MD, PhD

Source:Medicinenet.com.

Medical Author:

John P. Cunha, DO, FACOEP

Medical Editor:

William C. Shiel Jr., MD, FACP, FACR

Angina

2012-03-17T04:16:00.001-07:00

Introduction to angina

Chest pain is a common symptom that is caused by many different conditions. Some causes require prompt medical attention, such as angina, heart attack, or tearing of the aorta. Other causes of chest pain that may not require immediate medical intervention include spasm of the esophagus, gallbladder attack, or inflammation of the chest wall. An accurate diagnosis is important in providing proper treatment to patients with chest pain.
The diagnosis and treatment of angina is discussed below, as well as the diagnosis of other causes of chest pain that can mimic angina.

What is angina, and what are the symptoms of angina?

Angina (angina pectoris - Latin for squeezing of the chest) is chest discomfort that occurs when there is a decreased blood oxygen supply to an area of the heart muscle. In most cases, the lack of blood supply is due to a narrowing of the coronary arteries as a result of arteriosclerosis.
Angina is usually felt as:

pressure,
heaviness,
tightening,
squeezing, or
aching across the chest, particularly behind the breastbone.

This pain often radiates to the neck, jaw, arms, back, or even the teeth.
Patients may also suffer:

indigestion,
heartburn,
weakness,
sweating,
nausea,
cramping, and
shortness of breath.

Angina usually occurs during exertion, severe emotional stress, or after a heavy meal. During these periods, the heart muscle demands more blood oxygen than the narrowed coronary arteries can deliver. Angina typically lasts from 1 to 15 minutes and is relieved by rest or by placing a nitroglycerin tablet under the tongue. Nitroglycerin relaxes the blood vessels and lowers blood pressure. Both rest and nitroglycerin decrease the heart muscles demand for oxygen, thus relieving angina.
Angina is classified in one of two types: 1) stable angina or 2) unstable angina.
Stable angina
Stable angina is the most common type of angina, and what most people mean when they refer to angina. People with stable angina have angina symptoms on a regular basis and the symptoms are somewhat predictable (for example, walking up a flight of steps causes chest pain). For most patients, symptoms occur during exertion and commonly last less than five minutes. They are relieved by rest or medication, such as nitroglycerin under the tongue.
Unstable angina
Unstable angina is less common and more serious. The symptoms are more severe and less predictable than the pattern of stable angina. Moreover, the pains are more frequent, last longer, occur at rest, and are not relieved by nitroglycerin under the tongue (or the patient needs to use more nitroglycerin than usual). Unstable angina is not the same as a heart attack, but it warrants an immediate visit to your healthcare provider or hospital emergency department as further cardiac testing is urgently needed. Unstable angina is often a precursor to a heart attack.

What causes angina?

The most common cause of angina is coronary artery disease. A less common cause of angina is spasm of the coronary arteries.
Coronary artery disease
Coronary arteries supply oxygenated blood to the heart muscle. Coronary artery disease develops as cholesterol is deposited in the artery wall, causing the formation of a hard, thick substance called cholesterol plaque. The accumulation of cholesterol plaque over time causes narrowing of the coronary arteries, a process called arteriosclerosis. Arteriosclerosis can be accelerated by smoking, high blood pressure, elevated cholesterol, and diabetes. When coronary arteries become narrowed by more than 50% to 70%, they can no longer meet the increased blood oxygen demand by the heart muscle during exercise or stress. Lack of oxygen to the heart muscle causes chest pain (angina).
Coronary artery spasm
The walls of the arteries are surrounded by muscle fibers. Rapid contraction of these muscle fibers causes a sudden narrowing (spasm) of the arteries. A spasm of the coronary arteries reduces blood to the heart muscle and causes angina. Angina as a result of a coronary artery spasm is called "variant" angina or Prinzmetal angina. Prinzmetal angina typically occurs at rest, usually in the early morning hours. Spasms can occur in normal coronary arteries as well as in those narrowed by arteriosclerosis.
Coronary artery spasm can also be caused by use/abuse of cocaine. The spasm of the artery wall caused by cocaine can be so significant that it can actually cause a heart attack.

What are other causes of chest pain?

In caring for patients with chest pain, the doctor distinguishes whether the pain is related to a lack of oxygen to the heart muscle (as in angina or heart attack), or is due to another process. Many conditions are considered that can cause chest pain which is similar to that of a heart attack or angina. Examples include the following:

Pleuritis (pleurisy): Inflammation of the lining of the lungs (pleuritis) causes sharp chest pain, which is aggravated by deep breathing and coughing. Patients often notice shortness of breath, in part due to their shallow breathing to minimize chest pain. Viral infections are the most common causes of pleurisy. Other systemic inflammatory conditions, such as systemic lupus, can also cause pleurisy.
Pericarditis: Pericarditis is inflammation of the lining around the heart. Symptoms of pericarditis are similar to that of pleuritis.
Pneumonia: Pneumonia (bacterial infection of the lung) causes fever and chest pain. Chest pain in bacterial pneumonia is due to an irritation or infection of the lining of the lung (pleura).
Pulmonary embolism: blood clots travel from the veins of the pelvis or the lower extremities to the lung, the condition is called pulmonary embolism. Pulmonary embolism can cause death of lung tissue (pulmonary infarction). Pulmonary infarction can lead to irritation of the pleura, causing chest pain similar to pleurisy. Some common causes of blood clots in these veins is deep vein thrombosis (prolonged immobility, recent surgery, trauma to the legs, or pelvic infection).
Pneumothorax: Small sacs in the lung tissue (alveoli) can spontaneously burst, causing pneumothorax. Symptoms of pneumothorax include sudden, severe, sharp chest pain and shortness of breath. One common cause of pneumothorax is severe emphysema.
Mitral valve prolapse: Mitral valve prolapse is a common heart valve abnormality, affecting 5% to 10% of the population. MVP is especially common among women between 20 to 40 years of age. Chest pain with MVP is usually sharp but not severe. Unlike angina, chest pain with MVP rarely occurs during or after exercise, and usually will not respond to nitroglycerin.
Aortic dissection: The aorta is the major vessel delivering blood from the left ventricle to the rest of the body. Aortic dissection (tearing of the aorta wall) is a life-threatening emergency. Aortic dissection causes severe, unrelenting chest and back pain. Young adults with aortic dissection usually have Marfan's syndrome, an inherited disease in which an abnormal form of the structural protein called collagen causes weakness of the aortic wall. Older patients develop aortic dissection typically as a result of chronic, high blood pressure, in addition to generalized hardening of the arteries (arteriosclerosis).
Costochondritis, rib fractures, muscle strain or spasm: Pain originating from the chest wall may be due to muscle strain or spasm, costochondritis, or rib fractures. Chest wall pain is usually sharp and constant. It is usually worsened by movement, coughing, deep breathing, and direct pressure on the area. Muscle spasm and strain can result from vigorous, unusual twisting and bending. The joints between the ribs and cartilage next to the breastbone can become inflamed, a condition called costochondritis. Fractured ribs resulting from trauma or cancer involvement can cause significant chest pain.
Nerve compression: Compression of the nerve roots by bone spurs as they exit the spinal cord can cause pain. Nerve compression can also cause weakness and numbness in the upper arm and chest.
Shingles (herpes zoster infection of the nerves): Shingles is nerve irritation from the infection, which can cause chest pain days before any typical rash appears.
Esophageal spasm and reflux: The esophagus is the long muscular tube connecting the mouth to the stomach. Reflux, or regurgitation of stomach contents and acid into the esophagus can cause heartburn and chest pain. Spasm of the muscle of the esophagus can also cause chest pain which can be indistinguishable from chest pain caused by angina or a heart attack. The cause of esophageal muscle spasm is not known. Pain of esophageal spasm can respond to nitroglycerin in a similar manner as angina.
Gallbladder attack (gallstones): Gallstones can block the gallbladder or bile ducts and cause severe pain of the upper abdomen, back and chest. Gallbladder attacks can mimic the pain of angina and heart attack.
Anxiety and panic attacks: Anxiety, depression, and panic attacks are frequently associated with chest pain lasting from minutes to days. The pain can be sharp or dull. It is usually accompanied by shortness of breath, or the inability to take a deep breath. Emotional stress can aggravate chest pain, but the pain is generally not related to exertion, and is not relieved by nitroglycerin. These patients often breath too fast (hyperventilate), causing lightheadedness, numbness, and tingling in the lips and fingers. Coronary artery disease risk factors are typically absent in these patients. Since there is no test for panic attacks, patients with chest pain usually undergo tests to exclude coronary artery disease and other causes of chest pain.

Why is it important to establish the diagnosis of angina?

Angina is usually a warning sign of the presence of significant coronary artery disease. Patients with angina are at risk of developing a heart attack (myocardial infarction). A heart attack is the death of heart muscle precipitated by the complete blockage of a diseased coronary artery by a blood clot.
During angina, the lack of oxygen (ischemia) to the heart muscle is temporary and reversible. The lack of oxygen to the heart muscle resolves and the chest pain disappears when the patient rests. In contrast, the muscle damage in a heart attack is permanent. The dead muscle turns into scar tissue when healed. A scarred heart cannot pump blood as efficiently as a normal heart, and can lead to heart failure.
Up to 25% of patients with significant coronary artery disease have no symptoms at all, even though they clearly lack adequate blood and oxygen supply to the heart muscle. These patients have "silent" angina. They have the same risk of heart attack as those with symptoms of angina.

How is angina diagnosed?

The electrocardiogram (EKG, ECG) is a recording of the electrical activity of the heart muscle, and can detect heart muscle which is in need of oxygen. The EKG is useful in showing changes caused by inadequate oxygenation of the heart muscle or a heart attack.
Exercise stress test
In patients with a normal resting EKG, exercise treadmill or bicycle testing can be useful screening tools for coronary artery disease. During an exercise stress test (also referred to as stress test, exercise electrocardiogram, graded exercise treadmill test, or stress ECG), EKG recordings of the heart are performed continuously as the patient walks on a treadmill or pedals on a stationary bike at increasing levels of difficulty. The occurrence of chest pain during exercise can be correlated with changes on the EKG, which demonstrates the lack of oxygen to the heart muscle. When the patient rests, the angina and the changes on the EKG which indicate lack of oxygen to the heart can both disappear. The accuracy of exercise stress tests in the diagnosis of significant coronary artery disease is 60% to 70%. If the exercise stress test does not show signs of coronary artery disease, a nuclear agent (thallium) can be given intravenously during exercise stress test. The addition of thallium allows nuclear imaging of blood flow to different regions of the heart, using an external camera. A reduced blood flow in an area of the heart during exercise, with normal blood flow to the area at rest, signifies significant artery narrowing in that region of the heart.
Stress echocardiography
Stress echocardiography combines echocardiography (ultrasound imaging of the heart muscle) with exercise stress testing. Like the exercise thallium test, stress echocardiography is more accurate than an exercise stress test in detecting coronary artery disease. When a coronary artery is significantly narrowed, the heart muscle supplied by this artery does not contract as well as the rest of the heart muscle during exercise. Abnormalities in muscle contraction can be detected by echocardiography. Stress echocardiography and thallium stress tests are both about 80% to 85% accurate in detecting significant coronary artery disease.
When a patient cannot undergo exercise stress test because of neurological or orthopedic difficulties, medications can be injected intravenously to simulate the stress on the heart normally brought on by exercise. Heart imaging can be performed with a nuclear camera or echocardiography.
Cardiac catheterization
Cardiac catheterization with angiography (coronary arteriography) is a technique that allows x-ray pictures to be taken of the coronary arteries. It is the most accurate test to detect coronary artery narrowing. Small hollow plastic tubes (catheters) are advanced under x-ray guidance to the openings of the coronary arteries. Iodine contrast "dye" is injected into the arteries while an x-ray video is recorded. Coronary arteriography gives the doctor a picture of the location and severity of coronary artery disease. This information can be important in helping doctors select treatment options.
CT coronary angiogram
CT coronary angiography is procedure that uses an intravenous dye that contains iodine, and CT scanning to image the coronary arteries. While the use of catheters is not necessary (thus the term "noninvasive" test applies to this procedure), there are still some risks involved, including the following:

Patients allergic to iodine
Patients with abnormal kidney function
Radiation exposure which is similar to, if not greater than, that received with a conventional coronary angiogram.

Nonetheless, this is generally a very safe test for most people. It is a major tool in the diagnosis of coronary artery disease in patients:

at high risk for developing coronary disease (cigarette smokers, those with genetic risk, high cholesterol levels, hypertension, or diabetes),
who have unclear results with exercise stress tests or other testing, or
who have symptoms suspicious of coronary disease

What are the treatment options for angina patients?

Treatment options include:

rest,
medications (nitroglycerin, beta blockers, calcium channel blockers),
percutaneous transluminal coronary angioplasty (PTCA), or
coronary artery bypass graft surgery (CABG).

Angina medications

Nitroglycerin

Resting, nitroglycerin tablets (placed under the tongue), and nitroglycerin sprays all relieve angina by reducing the heart muscle's demand for oxygen. Nitroglycerin also relieves spasm of the coronary arteries and can redistribute coronary artery blood flow to areas that need it most. Short-acting nitroglycerin can be repeated at five minute intervals. When 3 doses of nitroglycerin fail to relieve the angina, further medical attention is recommended. Short-acting nitroglycerin can also be used prior to exertion to prevent angina.
Longer-acting nitroglycerin preparations, such as Isordil tablets, Nitro-Dur transdermal systems (patch form), and Nitrol ointment are useful in preventing and reducing the frequency and intensity of episodes in patients with chronic angina. The use of nitroglycerin preparations may cause headaches and lightheadedness due to an excess lowering of blood pressure.

Beta Blockers

Beta blockers relieve angina by inhibiting the effect of adrenaline on the heart. Inhibiting adrenaline decreases the heart rate, lowers the blood pressure, and reduces the pumping force of the heart muscle, all of which reduce the heart muscle's demand for oxygen. Examples of beta blockers include:

acebutolol (Sectral)
atenolol (Tenormin)
bisoprolol (Zebeta)
metoprolol (Lopressor, Lopressor LA, Toprol XL)
nadolol (Corgard)
propranolol (Inderal)
timolol (Blocadren)

Side effects include of beta blockers include:

worsening of asthma,
excess lowering of the heart rate and blood pressure,
depression,
fatigue,
impotence,
increased cholesterol levels, and
shortness of breath due to diminished heart muscle function (congestive heart failure).

Calcium Channel Blockers

Calcium channel blockers relieve angina by lowering blood pressure, and reducing the pumping force of the heart muscle, thereby reducing muscle oxygen demand. Calcium channel blockers also relieve coronary artery spasm. Examples of calcium channel blockers include:

amlodipine (Norvasc)
bepridil (Vascor)
diltiazem (Cardizem)
felodipine (Plendil)
isradipine (Dynacirc)
nicardipine, (Cardene)
nifedipine (Adalat, Procardia)
nimodipine (Nimotop)
nisoldipine (Sular)
verapamil (Calan)

Side effects of calcium channel blockers include:

swelling of the legs,
excess lowering of the heart rate and blood pressure, and
depressing heart muscle function.

Other anti-anginal drugs

Ranolazine (Ranexa) is indicated for the treatment of chronic angina. Ranexa may be used with beta-blockers, nitrates, calcium channel blockers, antiplatelet therapy, lipid-lowering therapy, ACE inhibitors, and angiotensin receptor blockers.

Angioplasty and coronary artery bypass surgery

When patients continue to have angina despite maximally tolerated combinations of nitroglycerin medications, beta blockers and calcium channel blockers, cardiac catheterization with coronary arteriography is indicated. Depending on the location and severity of the disease in the coronary arteries, patients can be referred for balloon angioplasty (percutaneous transluminal coronary angioplasty or PTCA) or coronary artery bypass graft surgery (CABG) to increase coronary artery blood flow.

What are other methods are used to evaluate angina?

Computerized X-ray scan (ultrafast CT scan) is highly accurate in detecting small amounts of calcium in the plaque of coronary arteries. If an ultrafast CT scan shows no calcium in the arteries, atherosclerotic coronary artery disease is unlikely. Ultrafast CT scanning is useful in evaluating chest pain in younger patients (men under 40 and women under 50 years old). Since young people do not normally have significant coronary artery plaque, a negative ultrafast CT scan makes the diagnosis of coronary artery disease unlikely. However, finding calcium by this method is less meaningful in older patients who are likely to have mild plaquing simply from the aging process.
Even though an ultrafast CT scan is useful in detecting calcium in plaque, it cannot determine whether the calcium-laden plaque actually causes artery narrowing and reduces blood flow. For example, a patient with a densely calcified plaque causing minimal or no artery narrowing will have a strongly positive ultrafast CT scan but a normal exercise treadmill test. In most patients who are suspected of having angina due to coronary artery disease, an exercise treadmill study is usually the first step in determining whether any plaque is clinically significant. Newer very high speed CT scanners can actually detect true coronary artery plaques and lesions similar to coronary angiography.
Magnetic resonance imaging (MRI), using magnetism and radio waves, can be used to image (produce a likeness of) the blood vessels. Currently, the larger vessels, such as the carotid arteries in the neck, can be imaged using this technique. Future software and hardware improvements may allow screening of the heart's arteries with magnetic resonance testing.

What's new in the treatment of angina and heart attacks?

Coronary arteries can close after angioplasty, causing recurrent angina or even heart attacks. One way to decrease the risk of coronary artery closure is by deploying stents to keep the arteries open. Drug-coated stents are being improved to significantly reduce the rate of artery closure.

Angina At A Glance

Angina is one of many causes of chest pain.
Angina is chest pain that is a result of inadequate oxygen supply to the heart muscle.
Angina can be caused by coronary artery disease or spasm of the coronary arteries.
EKG, exercise stress test, stress echocardiography, stress thallium, and cardiac catheterization are important in the diagnosis of angina.
Treatment of angina includes rest, medications, angioplasty, and/or coronary artery bypass surgery.

Additional resources from WebMD Boots UK on Heart Disease: Angina

REFERENCE:
UpToDate.com. Transmyocardial laser revascularization for management of refractory angina.

FDA Prescribing Information for Ranexa.

Source:Medicinenet.com.

Medical Author:

John P. Cunha, DO, FACOEP

Medical Editor:

Daniel Lee Kulick, MD, FACC, FSCAI

Medical Editor:

William C. Shiel Jr., MD, FACP, FACR

Sudden Cardiac Arrest (Sudden Cardiac Death)

2012-03-17T04:13:00.001-07:00

Introduction to sudden cardiac arrest

A natural disaster hits, the power goes off and the lights go out. It's a common scene that plays out during hurricane and tornado seasons, and it's very similar in trying to explain sudden cardiac arrest. The heart sustains an insult, the electricity is short circuited, the heart can't pump, and the body dies.
The heart is an electrical pump, where the electricity is generated in special pacemaker cells in the upper chamber, or atrium, of the heart. This electrical spark is carried through pathways in the heart so that all the muscle cells contract at once and produce a heart beat. This pumps blood through the heart valves and into all the organs of the body so that they can do their work.
This mechanism can break down in a variety of ways, but the final pathway in sudden death is the same: the electrical system is irritated and fails to produce electrical activity that causes the heart to beat. The heart muscle can't supply blood to the body, particularly the brain, and the body dies. Ventricular fibrillation (V Fib) is the most common reason for sudden death in patients. Without a coordinated electrical signal, the bottom chambers of the heart (ventricles) stop beating and instead, jiggle like Jello. Ventricular Fibrillation is treated with electrical shock, but for it to be effective, the shock usually needs to happen within less than four to six minutes, not only for it to be effective, but also to minimize brain damage from lack of blood and oxygen supply. Automatic external defibrillators (AEDs) are commonly available in public places to allow almost anybody to treat sudden death. Less commonly, the heart can just stop beating. The absence of a heart beat is known as asystole (asystole: a=no + systole=beat).

What are the causes of sudden cardiac arrest?

Sudden death is most often caused by heart disease. When blood vessels narrow, the heart muscle can become irritated because of lack of blood supply. In heart attack (acute myocardial infarction), a blood vessel becomes completely blocked by a blood clot, and there is enough irritability of the muscle to cause ventricular fibrillation. In fact, the reason many people with chest pain are admitted to the hospital is to monitor their heart rate and rhythm for signs that might lead to ventricular fibrillation. Sudden death may also be the first presentation of heart disease.
Congestive heart failure and heart valve problems, like aortic stenosis (narrowing of the aortic valve) also increase the risk of sudden cardiac arrest.
Cardiomyopathy is a broad category of heart disease where the heart muscle does not contract properly for whatever reason. Often it is ischemic, where part of the heart muscle doesn't get an adequate blood supply for a prolonged period of time and no longer can efficiently pump blood. People whose ejection fractions (the amount of blood pumped out of the heart with each heart beat) is less than 30% are at greater risk for sudden death (a normal ejection fraction is above 50%). In some people, cardiomyopathy may develop in the absence of ischemic heart disease.
Inflammation of the heart muscle, known as myocarditis (myo=muscle + card=heart + itis= inflammation), can also cause rhythm disturbances. Diseases like sarcoidosis, amyloidosis, and infections can cause inflammation of the heart muscle.
Some people are born with electrical conducting systems that are faulty, which place them at higher risk for rhythm disturbances. Some are due to the wiring, or electrical conduction system, like Wolff-Parkinson-White syndrome, while others are due to the structural basic structural problems within the heart, like Marfan syndrome.
Pulmonary embolus, a blood clot to the lung, can also cause sudden death. Clots form in the leg or arm and may break off and flow to the lung where they decrease the lung's ability to get oxygen from the air to the body. Risk factors for blood clots include surgery, prolonged immobilization (for example, hospitalization, long car rides or plane trips), trauma, or certain diseases like cancer.
Blunt chest trauma, such is in a motor vehicle accident, may result in ventricular fibrillation. (please see commotio cordis below)

What about sudden cardiac arrest in the young?

In younger people, sudden death is a rare event, but since it often involves people involved in athletics, cases are often reported in the press. The most common cause is hypertrophic cardiomyopathy (hypertrophy=to grow abnormally large + cardio=heart + myopathy = diseased muscle). This disease is often hereditary, and the walls of the ventricle are larger than they should be. This makes the pumping chamber of the heart smaller, and the heart has to work harder to pump blood out of the heart. As well, the thickened muscle narrows the space for the blood to flow through the aortic valve and to the rest of the body. During exercise, this decreased blood flow can irritate the heart muscle itself and cause ventricular fibrillation, collapse, and sudden death.
Anomalous coronary arteries can also cause sudden death in the young. The heart is a muscle itself, and like any muscle, it needs blood supply to provide oxygen for it to work. Normally, the coronary arteries lie on the surface of the heart. Anomalous arteries dive into the heart muscle itself and may be occluded when the heart muscle that surrounds the abnormally placed artery squeezes aggressively, as with exercise, shutting off blood supply to part of the heart. This irritates the electrical system and can cause ventricular fibrillation and sudden death.
The pre-participation athletic physical examination is a useful tool to screen children and adolescents for their risk of sudden cardiac arrest.
Commotio cordis is a situation in which the heart stops when the chest is hit by an object. News stories occasionally report of baseball players who are hit in the chest by a ball and collapse because their heart stops beating. The heart sits behind the breastbone, and the electrical system can be short circuited when a direct blow is sustained.

What are the symptoms of sudden cardiac arrest?

In sudden cardiac arrest, the heart stops beating, and blood is not supplied to the body. The presentation is not subtle. Almost immediate loss of consciousness occurs, and the affected person will not be able to be aroused. The person will fall or slump over. No pulse will be able to be palpated, and there will be no signs of breathing.

What is the diagnosis for sudden cardiac arrest?

Sudden cardiac arrest is an unexpected death in a person who had no known previous diagnosis of a fatal disease or condition. The person may or may not have heart disease.

What is the treatment for sudden cardiac arrest?

The vast majority of people whose heart stops beating unexpectedly have ventricular fibrillation. The definitive treatment for this is defibrillation using electricity to shock the heart back into a regular rhythm. With technological advances, AEDs are now a routine sight wherever people congregate.
Communities which institute public CPR education, use of AEDs, and rapid activation of 911 emergency medical services have dramatically increased survival rates from sudden cardiac arrest. Unfortunately, because the brain is so sensitive to the lack of oxygen and blood flow, unless treatment occurs within four to six minutes, there is a high risk of some permanent brain damage.
Should the patient survive to be transported to the hospital, the reason for collapse and sudden death will need to be diagnosed. Regardless, the ABCs of resuscitation will be re-evaluated. Airway, Breathing, and Circulation (heart beat and blood pressure) will be supported, and admission to an intensive care unit is most likely.
Diagnostic tests may include repeated electrocardiograms (EKGs), echocardiogram (ultrasounds of the heart), and cardiac catheterization and electrophysiologic studies, in which the electrical pathways of the heart are mapped.
Recent research involving the treatment of survivors of cardiac arrest suggests that prompt institution of hypothermia (cooling of the body) may prevent or lessen the degree of brain injury.
Survivors of sudden cardiac arrest are often candidates for implantable cardiac defibrillators.

Can sudden cardiac arrest be prevented?

Death is best treated by prevention. Most sudden death is associated with heart disease, so the at-risk population remains males older than 40 years of age who smoke, have high blood pressure, and diabetes (the risk factors for heart attack). Other risks include syncope (fainting or loss of consciousness) and known heart disease.
Syncope, or loss of consciousness, is a significant risk factor for sudden death. While some reasons for passing out are benign, there is always a concern that the reason was an abnormal heart rhythm that subsequently spontaneously corrected. The fear is that the next episode will be a sudden cardiac arrest. Depending on the healthcare provider's suspicion based on the patient's history, physical examination, laboratory tests, and EKG, the healthcare practitioner may recommend inpatient or outpatient heart monitoring to try to find a clue as to whether the passing out was due to a deadly heart rhythm. Unfortunately, the potentially suspect rhythm may not recur and depending on the situation, prolonged outpatient monitoring lasting weeks and months may be necessary. Use of electrophysiologic testing may help identify high risk patients (the electrical pathways are mapped using techniques similar to heart catheterization).
In people who present to their doctor with chest pain, aside from making the diagnosis, monitoring both the heart rate and rhythm are emphasized. The purpose of watching people with chest pain in a hospital setting is to prevent sudden cardiac arrest.
Using implantable defibrillators in high risk patients, especially those with markedly decreased ejection fractions can reduce the incidence of sudden cardiac arrest. These devices are placed under the skin in the chest wall and have wires that are attached to the heart itself. When they detect ventricular fibrillation, a shock is automatically delivered to the heart, restoring a heart beat and averting sudden death.

What is the prognosis for sudden cardiac arrest?

The frequency of sudden cardiac arrest is related to the frequency of coronary artery disease. If public health initiatives work to decrease risk the factors for heart disease, the risk for sudden death should decrease as well.
In the adolescent population, increased awareness of hypertrophic cardiomyopathy and appropriate screening may decrease the frequency of sudden death.
Public education and widespread availability of AEDs will increase survival.
Source:Medicinenet.com.

Medical Author:

Benjamin Wedro, MD, FACEP, FAAEM

Medical Editor:

Daniel Lee Kulick, MD, FACC, FSCAI

Medical Editor:

Melissa Conrad Stöppler, MD

Low Blood Pressure (Hypotension)

2012-03-17T04:11:00.001-07:00

What is low blood pressure?

Blood pressure is the force exerted by circulating blood on the walls of blood vessels. It constitutes one of the critically important signs of life or vital signs which include heart beat, breathing, and temperature. Blood pressure is generated by the heart pumping blood into the arteries modified by the response of the arteries to the flow of blood.
An individual's blood pressure is expressed as systolic/diastolic blood pressure, for example, 120/80.The systolic blood pressure (the top number) represents the pressure in the arteries as the muscle of the heart contracts and pumps blood into them. The diastolic blood pressure (the bottom number) represents the pressure in the arteries as the muscle of the heart relaxes following its contraction. Blood pressure always is higher when the heart is pumping (squeezing) than when it is relaxing.
The range of systolic blood pressure for most healthy adults falls between 90 and 120 millimeters of mercury (mm Hg). Normal diastolic blood pressure ranges between 60 and 80 mm Hg. Current guidelines define normal blood pressure range as lower than 120/80. Blood pressures over 130/80 are considered high. High blood pressure increases the risk of developing:

heart disease,
kidney disease,
hardening of the arteries (atherosclerosis or arteriosclerosis),
eye damage, and
stroke.

Low blood pressure (hypotension) is pressure so low it causes symptoms or signs due to the low flow of blood through the arteries and veins. When the flow of blood is too low to deliver enough oxygen and nutrients to vital organs such as the brain, heart, and kidney, the organs do not function normally and may be temporarily or permanently damaged.
Unlike high blood pressure, low blood pressure is defined primarily by signs and symptoms of low blood flow and not by a specific blood pressure number. Some individuals routinely may have blood pressures of 90/50 with no symptoms and therefore do not have low blood pressure. However, others who normally have higher blood pressures may develop symptoms of low blood pressure if their blood pressure drops to 100/60.

How is blood pressure generated?

During relaxation of the heart (diastole) the left ventricle of the heart fills with blood returning from the lungs. The left ventricle then contracts and pumps blood into the arteries (systole). The blood pressure in the arteries during contraction of the ventricle (systolic pressure) is higher because blood is being actively ejected into the arteries. It is lower during relaxation of the ventricle (diastolic pressure) when no blood is being ejected into the arteries. The pulse that we can feel when we place our fingers over an artery is caused by the contraction of the left ventricle and the ejection of blood.
Blood pressure is determined by two factors: 1) The amount of blood pumped by the left ventricle of the heart into the arteries, and 2) the resistance to the flow of blood caused by the walls of the arterioles (smaller arteries).
Generally, blood pressure tends to be higher if more blood is pumped into the arteries or if the arterioles are narrow and/or stiff. (Narrow and/or stiff arterioles, by resisting the flow of blood, increase blood pressure.) Arterioles may become narrower when the muscles surrounding them contract. Arterioles may become stiff and narrow when older patients develop atherosclerosis.
Blood pressure tends to be lower if less blood is being pumped into the arteries or if the arterioles are larger and more flexible and, therefore, have less resistance to the flow of blood.

How does the body maintain normal blood pressure?

The body has mechanisms to alter or maintain blood pressure and blood flow. There are sensors that sense blood pressure in the walls of the arteries and send signals to the heart, the arterioles, the veins, and the kidneys that cause them to make changes that lower or increase blood pressure. There are several ways in which blood pressure can be adjusted - by adjusting the amount of blood pumped by the heart into the arteries (cardiac output), the amount of blood contained in the veins, the arteriolar resistance, and the volume of blood.

The heart can speed up and contract more frequently and it can eject more blood with each contraction. Both of these responses increase the flow of blood into the arteries and increase blood pressure.

The veins can expand and narrow. When veins expand, more blood can be stored in the veins and less blood returns to the heart for pumping into the arteries. As a result, the heart pumps less blood, and blood pressure is lower. On the other hand, when veins narrow, less blood is stored in the veins, more blood returns to the heart for pumping into the arteries, and blood pressure is higher.

The arterioles can expand and narrow. Expanded arterioles create less resistance to the flow of blood and decrease blood pressure, while narrowed arterioles create more resistance and raise blood pressure.

The kidney can respond to changes in blood pressure by increasing or decreasing the amount of urine that is produced. Urine is primarily water that is removed from the blood. When the kidney makes more urine, the amount (volume) of blood that fills the arteries and veins decreases, and this lowers blood pressure. If the kidneys make less urine, the amount of blood that fills the arteries and veins increases and this increases blood pressure. Compared with the other mechanisms for adjusting blood pressure, changes in the production of urine affect blood pressure slowly over hours and days. (The other mechanisms are effective in seconds.)

For example, low blood volume due to bleeding (such as a bleeding ulcer in the stomach or from a severe laceration from an injury) can cause low blood pressure. The body quickly responds to the low blood volume and pressure by the following adjustments which all increase blood pressure:

The heart rate increases and the forcefulness of the heart's contractions increase thus pumping more blood through the heart.

Veins narrow to return more blood to the heart for pumping.

Blood flow to the kidneys decreases to reduce the formation of urine and thereby increases the volume of blood in the arteries and veins.

Arterioles narrow to increase resistance to blood flow

These adaptive responses will keep the blood pressure in the normal range unless blood loss becomes so severe that the responses are overwhelmed.

Is low blood pressure bad for your health?

People who have lower blood pressures have a lower risk of stroke, kidney disease, and heart disease. Athletes, people who exercise regularly, people who maintain ideal body weight, and non-smokers tend to have lower blood pressures. Therefore, low blood pressure is desirable as long as it is not low enough to cause symptoms and damage to the organs in the body.

What are low blood pressure signs and symptoms?

When blood pressure is not sufficient to deliver enough blood to the organs of the body, the organs do not work properly and can be temporarily or permanently damaged. For example, if insufficient blood flows to the brain, brain cells do not receive enough oxygen and nutrients, and a person can feel lightheaded, dizzy, or even faint.
Going from a sitting or lying position to a standing position often brings out symptoms of low blood pressure. This occurs because standing causes blood to "settle" in the veins of the lower body, and this can lower the blood pressure. If the blood pressure is already low, standing can make the low pressure worse, to the point of causing symptoms. The development of lightheadedness, dizziness, or fainting upon standing caused by low blood pressure is called orthostatic hypotension. Normal individuals are able to compensate rapidly for the low pressure created by standing with the responses discussed previously and do not develop orthostatic hypotension.
When there is insufficient blood pressure to deliver blood to the coronary arteries (the arteries that supply blood to the heart's muscle), a person may develop chest pain (a symptom of angina) or even a heart attack.
When insufficient blood is delivered to the kidneys, the kidneys fail to eliminate wastes from the body, for example, urea (BUN) and creatinine, and increases in their levels in the blood occur.
Shock is a life-threatening condition where persistently low blood pressure causes organs such as kidney(s), liver, heart, lung, and brain to fail rapidly.

What are the causes of low blood pressure?

Conditions that reduce the volume of blood, reduce cardiac output (the amount of blood pumped by the heart), and medications are frequent reasons for low blood pressure.

Dehydration is common among patients with prolonged nausea, vomiting, and diarrhea. Large amounts of water are lost when vomiting and with diarrhea, especially if the person does not drink adequate amounts of fluid to replace the depleted water.

Other causes of dehydration include exercise, sweating, fever, and heat exhaustion, or heat stroke. Individuals with mild dehydration may experience only thirst and dry mouth. Moderate to severe dehydration may cause orthostatic hypotension (manifested by lightheadedness, dizziness, or fainting upon standing). Prolonged and severe dehydration can lead to shock, kidney failure, confusion, acidosis (too much acid in the blood), coma, and even death.

Moderate or severe bleeding can quickly deplete an individual's body of blood, leading to low blood pressure or orthostatic hypotension. Bleeding can result from trauma, surgical complications, or from gastrointestinal abnormalities such as ulcers, tumors, or diverticulosis. Occasionally, the bleeding may be so severe and rapid (for example, bleeding from a ruptured aortic aneurysm) that it causes shock and death rapidly.

Severe inflammation of organs inside the body such as acute pancreatitis can cause low blood pressure. In acute pancreatitis, fluid leaves the blood vessels to enter the inflamed tissues around the pancreas as well as the abdominal cavity, concentrating blood and reducing its volume.

Causes of low blood pressure due to heart disease

Weakened heart muscle can cause the heart to fail and reduce the amount of blood it pumps. One common cause of weakened heart muscle is the death of a large portion of the heart's muscle due to a single, large heart attack or repeated smaller heart attacks. Other examples of conditions that can weaken the ability of the heart to pump blood include medications that are toxic to the heart, infections of the muscle of the heart by viruses (myocarditis), and diseases of the heart's valves such as aortic stenosis.

Pericarditis is an inflammation of the pericardium (the sac surrounding the heart). Pericarditis can cause fluid to accumulate within the pericardium and compress the heart, restricting the ability of the heart to fill and pump blood.

Pulmonary embolism is a condition in which a blood clot in a vein (deep vein thrombosis) breaks off and travels to the heart and eventually the lung. A large blood clot can block the flow of blood into the left ventricle from the lungs and severely diminish the blood returning to the heart for pumping. Pulmonary embolism is a life-threatening emergency.

A slow heart rate (bradycardia) can decrease the amount of blood pumped by the heart. The resting heart rate for a healthy adult is between 60 and 100 beats/minute. Bradycardia (resting heart rates slower than 60 beats/minute) does not always cause low blood pressure. In fact, some highly trained athletes can have resting heart rates in the 40s and 50s (beats per minute) without any symptoms. (The slow heart rates are offset by more forceful contractions of the heart that pump more blood than in non-athletes.) But in many patients bradycardia can lead to low blood pressure, lightheadedness, dizziness, and even fainting.

Several common reasons for bradycardia include: 1) sick sinus syndrome, 2) heart block, and 3) drug toxicity. Many of these conditions occur in the elderly.
Sick sinus syndrome: Sick sinus syndrome occurs when the diseased electrical system of the heart cannot generate signals fast enough to maintain a normal heart rate.
Heart block: Heart block occurs when the specialized tissues that transmit electrical current in the heart are damaged by heart attacks, degeneration from atherosclerosis, and medications. Heart block prevents some or all of the electrical signals from reaching parts of the heart, and this prevents the heart from contracting as well as it otherwise would.
Drug toxicity: Drugs such as digoxin (Lanoxin) or beta blockers for high blood pressure, can slow the transmission of electricity in the heart chemically and can cause bradycardia and hypotension (see section below "Medications that cause low blood pressure").

An abnormally fast heart rate (tachycardia) also can cause low blood pressure. The most common example of tachycardia causing low blood pressure is atrial fibrillation. Atrial fibrillation is a disorder of the heart characterized by rapid and irregular electrical discharges from the muscle of the heart causing the ventricles to contract irregularly and (usually) rapidly. The rapidly contracting ventricles do not have enough time to fill maximally with blood before the each contraction, and the amount of blood that is pumped decreases in spite of the faster heart rate. Other abnormally rapid heart rhythms such as ventricular tachycardia also can produce low blood pressure, sometimes even life-threatening shock.

Medications that cause low blood pressure

Medications such as calcium channel blockers, beta blockers, and digoxin (Lanoxin) can slow the rate at which the heart contracts. Some elderly people are extremely sensitive to these medications since they are more likely to have diseased hearts and electrical conduction tissues. In some individuals, the heart rate can become dangerously slow even with small doses of these medications.

Medications used in treating high blood pressure (such as ACE inhibitors, angiotensin receptor blockers, beta blockers, calcium channel blockers, and alpha-blockers) can excessively lower blood pressure and result in symptomatic low blood pressure especially among the elderly.

Water pills (diuretics) such as hydrochlorothiazide furosemide (Lasix) can decrease blood volume by causing excessive urination.

Medications used for treating depression, such as amitriptyline (Elavil), Parkinson's disease, such as levodopa-carbidopa (Sinemet), erectile dysfunction (impotence), such as sildenafil (Viagra), vardenafil (Levitra), and tadalafil (Cialis) when used in combination with nitroglycerine, can cause low blood pressure.

Alcohol and narcotics also can cause low blood pressure.

Other conditions that cause low blood pressure

Vasovagal reaction is a common condition in which a healthy person temporarily develops low blood pressure, slow heart rate, and sometimes fainting. A vasovagal reaction typically is brought on by emotions of fear or pain such as having blood drawn, starting an intravenous infusion, or by gastrointestinal upset. Vasovagal reactions are caused by activity of the involuntary (autonomic) nervous system, especially the vagus nerve, which releases hormones that slow the heart and widen the blood vessels. The vagus nerve also controls digestive tract function and senses activity in the digestive system. Thus, some people can have a vasovagal reaction from straining at a bowel movement or vomiting.

Postural (orthostatic) hypotension is a sudden drop in blood pressure when an individual stands up from a sitting, squatting, or supine (lying) position. When a person stands up, gravity causes blood to settle in the veins in the legs so that less blood returns to the heart for pumping, and, as a result, the blood pressure drops. The body normally responds automatically to the drop in blood pressure by increasing the rate at which the heart beats and by narrowing the veins to return more blood to the heart. In patients with postural hypotension, this compensating reflex fails to occur, resulting low blood pressure and its symptoms. Postural hypotension can occur in persons of all ages but is much more common among the elderly, especially in those on medications for high blood pressure and/or diuretics. Other causes of postural hypotension include dehydration, adrenal insufficiency (discussed later), prolonged bed rest, diabetes that has caused damage to the autonomic nerves, alcoholism with damage to the autonomic nerves, and certain rare neurological syndromes (for example, Shy-Drager syndrome) that damage the autonomic nerves.

Another form of postural hypotension occurs typically in young healthy individuals. After prolonged standing, the individual's heart rate and blood pressure drop, causing dizziness, nausea, and often fainting. In these individuals, the autonomic nervous system wrongly responds to prolonged standing by directing the heart to slow down and the veins to dilate.

Micturition syncope is a temporary drop in blood pressure and loss of consciousness brought about by urinating. This condition typically occurs in elderly patients and may be due to the release by the autonomic nerves of hormones that lower blood pressure.

Adrenal insufficiency, for example, due to Addison's disease, can cause low blood pressure. Addison's disease is a disorder in which the adrenal glands (small glands next to the kidneys) are destroyed. The destroyed adrenal glands can no longer produce sufficient adrenal hormones (specifically cortisol) necessary to maintain normal bodily functions. Cortisol has many functions, one of which is to maintain blood pressure and the function of the heart. Addison's disease is characterized by weight loss, muscle weakness, fatigue, low blood pressure, and, sometimes, darkening of the skin.

Septicemia is a severe infection in which bacteria (or other infectious organisms such as fungi) enter the blood. The infection typically originates in the lungs (as pneumonia), bladder, or in the abdomen due to diverticulitis or gallstones. The bacteria then enter the blood where they release toxins and cause life-threatening and profound low blood pressure (septic shock), often with damage to several organs.

Anaphylaxis (anaphylactic shock) is a potentially fatal allergic reaction to medications such as penicillin, intravenous iodine used in some X-ray studies, foods such as peanuts, or bee stings (insect stings). In addition to a severe drop in blood pressure, individuals may also experience hives as well as wheezing due to constriction of the airways, and a swollen throat which cause difficulty breathing. The shock is caused by enlargement of blood-containing blood vessels and escape of water from the blood into the tissues.

How is low blood pressure diagnosed and evaluated?

In some individuals, particularly relatively healthy ones, symptoms of weakness, dizziness, and fainting raise the suspicion of low blood pressure. In others, an event often associated with low blood pressure, for example a heart attack has occurred to cause the symptoms.
Measuring blood pressure, in both the lying (supine) and standing positions usually is the first step in diagnosing low blood pressure. In patients with symptomatic low blood pressure, there often is a marked drop in blood pressure upon standing, and patients may even develop orthostatic symptoms. The heart rate often increases greatly. Once low blood pressure has been identified as the cause of symptoms, the goal is to identify the cause of the low blood pressure. Sometimes the causes are readily apparent (such as loss of blood due to trauma, or sudden shock after receiving x-ray dyes containing iodine). At other times, the cause may be identified by testing:

CBC (complete blood count). CBC may reveal anemia from blood loss or elevated white blood cells due to infection.

Blood electrolyte measurements may show dehydration and mineral depletion, renal failure (kidney failure), or acidosis (excess acid in the blood).

Cortisol levels can be measured to diagnose adrenal insufficiency and Addison's disease.

Blood and urine cultures can be performed to diagnose septicemia and bladder infections, respectively.

Radiology studies, such as chest x-rays, abdominal ultrasounds, and computerized tomography (CT or CAT) scans may detect pneumonia, heart failure, gallstones, pancreatitis, and diverticulitis.

Electrocardiograms (EKG) can detect abnormally slow or rapid heart beats, pericarditis, and heart muscle damage from either previous heart attacks or a reduced supply of blood to the heart muscle that has not yet caused a heart attack.

Holter monitor recordings are used to diagnose intermittent episodes of abnormal heart rhythms. If abnormal rhythms occur intermittently, a standard EKG performed at the time of a visit to the doctor's office may not show the abnormal rhythm. A Holter monitor is a continuous recording of the heart's rhythm for 24 hours that often is used to chart and diagnose intermittent episodes of bradycardia or tachycardia.

Patient-activated event recorder. If the episodes of bradycardia or tachycardia are infrequent, a 24-hour Holter recording may not capture these sporadic episodes. In this situation, a patient can wear a patient-activated event recorder for up to four weeks. The patient presses a button to start the recording when he or she senses the onset of an abnormal heart rhythm or symptoms possibly caused by low blood pressure. The doctor then analyzes the recordings at a later date to identify the abnormal episodes.

Echocardiograms are examinations of the structures and motion of the heart using ultrasound. Echocardiograms can detect pericardial fluid due to pericarditis, the extent of heart muscle damage from heart attacks, diseases of the heart valves, and rare tumors of the heart.

Ultrasound examinations of the leg veins and CT scans of the chest can detect deep vein thrombosis and pulmonary embolism.

Tilt-Table tests are used to evaluate patients suspected of having postural hypotension or syncope due to abnormal function of the autonomic nerves. During a tilt-table test, the patient lies on an examining table with an intravenous infusion administered while the heart rate and blood pressure are monitored. The table then is tilted upright for 15 minutes to 45 minutes. Heart rate and blood pressure are monitored every few minutes. The purpose of the test is to try to reproduce postural hypotension. Sometimes a doctor may administer epinephrine (Adrenalin, Isuprel) intravenously to induce postural hypotension.

How is low blood pressure treated?

Low blood pressure in healthy subjects without symptoms or organ damage needs no treatment. However, all patients with symptoms possibly due to low blood pressure should be evaluated by a doctor. (Patients who have had a major drop in blood pressure from their usual levels even without the development of symptoms also should be evaluated.) The doctor needs to identify the cause of the low blood pressure; remedies will depend on the cause. For example, if a medication is causing the low blood pressure, the dose of medication may have to be reduced or the medication stopped, though only after consulting the doctor. Self-adjustment of medication should not be done.

Dehydration is treated with fluids and minerals (electrolytes). Mild dehydration without nausea and vomiting can be treated with oral fluids and electrolytes. Moderate to severe dehydration usually is treated in the hospital or emergency room with intravenous fluids and electrolytes.

Blood loss can be treated with intravenous fluids and blood transfusions. Continuous and severe bleeding needs to be treated immediately.

Septic shock is an emergency and is treated with intravenous fluids and antibiotics.

Blood pressure medications or diuretics are adjusted, changed, or stopped by the doctor if they are causing low blood pressure symptoms.

Bradycardia may be due to a medication. The doctor may reduce, change or stop the medication. Bradycardia due to sick sinus syndrome or heart block is treated with an implantable pacemaker.

Tachycardia is treated depending on the nature of the tachycardia. Atrial fibrillation can be treated with oral medications, electrical cardioversion, or a catheterization procedure called pulmonary vein isolation. Ventricular tachycardia can be controlled with medications or with an implantable defibrillator.

Pulmonary embolism and deep vein thrombosis is treated with blood thinners, intravenous initially with heparin, and oral warfarin (Coumadin) later.

Pericardial fluid can be removed by a procedure called pericardiocentesis.

Postural hypotension can be treated with changes in diet such as increasing water and salt intake*, increasing intake of caffeinated beverages (because caffeine constricts blood vessels), using compression stockings to compress the leg veins and reduce the pooling of blood in the leg veins, and in some patients, the use of a medication called midodrine (ProAmatine). The problem with ProAmatine is that while it increases blood pressure in the upright position, the supine blood pressure may become too high, thus increasing the risk of strokes. Mayo Clinic researchers found that a medication used to treat muscle weakness in myasthenia gravis called pyridostigmine (Mestinon) increases upright blood pressure but not supine blood pressure. Mestinon, an anticholinesterase medication, works on the autonomic nervous system, especially when a person is standing up. Side effects include minor abdominal cramping or increased frequency of bowel movements. *Note: Increasing salt intake can lead to heart failure in patients with existing heart disease and should not be undertaken without consulting a doctor.

Postprandial hypotension refers to low blood pressure occurring after meals. Ibuprofen (Motrin) or indomethacin (Indocin) may be beneficial.

Vasovagal Syncope can be treated with several types of drugs such as beta blockers [for example, propanolol (Inderal, Inderal LA)], selective serotonin reuptake inhibitors [fluoxetine (Prozac), escitalopram oxalate (Lexapro), paroxetine (Paxil), sertraline (Zoloft), citalopram (Celexa), fluvoxamine (Luvox)], fludrocortisone (Florinef) (a drug that prevents dehydration by causing the kidney(s) to retaining water). A pacemaker can also be helpful when a patient fails drug therapy.

Low Blood Pressure At A Glance

Low blood pressure, also called hypotension, is blood pressure that is low enough that the flow of blood to the organs of the body is inadequate and symptoms and/or signs of low blood flow develop.
Low pressure alone, without symptoms or signs, usually is not unhealthy.
The symptoms of low blood pressure include lightheadedness, dizziness, and fainting. These symptoms are most prominent when individuals go from the lying or sitting position to the standing position (orthostatic hypotension).
Low blood pressure that causes an inadequate flow of blood to the body's organs can cause strokes, heart attacks, and kidney failure. It's most severe form is shock.
Common causes of low blood pressure include a reduced volume of blood, heart disease, and medications.
The cause of low blood pressure can be determined with blood tests, radiologic studies, and cardiac testing to look for arrhythmias.
Treatment of low blood pressure is determined by the cause of the low pressure.

Additional resources from WebMD Boots UK on Low Blood Pressure

REFERENCES:

American Family Physician. Off-Label Applications for SSRIs.

Hilz MJ, Marthol H, Neundorfer B. "Syncope - a systematic overview of classification, pathogenesis, diagnosis and management," Fortschr Neurol Psychiatr. 2002 Feb;70(2):95-107.

Medlineplus.com. Vital Signs.

Park Nicollet Methodist Hospital.com. Postural Hypotension.

WebMD.com. Alpha Blocker Medications for Prostatitis.

Previous contributing author: Dennis Lee, MD

Source:Medicinenet.com.

Medical Author:

John P. Cunha, DO, FACOEP

Medical Editor:

Jay W. Marks, MD

Polycystic Kidney Disease (PKD)

2012-03-17T04:07:00.001-07:00

What is Polycystic Kidney Disease?

Polycystic kidney disease (PKD) is a genetic disorder characterized by the growth of numerous cysts in the kidneys. The kidneys are two organs, each about the size of a fist, located in the upper part of a person's abdomen, toward the back. The kidneys filter wastes and extra fluid from the blood to form urine. They also regulate amounts of certain vital substances in the body. When cysts form in the kidneys, they are filled with fluid. PKD cysts can profoundly enlarge the kidneys while replacing much of the normal structure, resulting in reduced kidney function and leading to kidney failure.
When PKD causes kidneys to fail-which usually happens after many years-the patient requires dialysis or kidney transplantation. About one-half of people with the most common type of PKD progress to kidney failure, also called end-stage renal disease (ESRD).
PKD can also cause cysts in the liver and problems in other organs, such as blood vessels in the brain and heart. The number of cysts as well as the complications they cause help doctors distinguish PKD from the usually harmless "simple" cysts that often form in the kidneys in later years of life.
In the United States, about 600,000 people have PKD, and cystic disease is the fourth leading cause of kidney failure. Two major inherited forms of PKD exist:

Autosomal dominant PKD is the most common inherited form. Symptoms usually develop between the ages of 30 and 40, but they can begin earlier, even in childhood. About 90 percent of all PKD cases are autosomal dominant PKD.
Autosomal recessive PKD is a rare inherited form. Symptoms of autosomal recessive PKD begin in the earliest months of life, even in the womb.

What is autosomal dominant PKD?

Autosomal dominant PKD is the most common inherited disorder of the kidneys. The phrase "autosomal dominant" means that if one parent has the disease, there is a 50 percent chance that the disease gene will pass to a child. In some cases-perhaps 10 percent-autosomal dominant PKD occurs spontaneously in patients. In these cases, neither of the parents carries a copy of the disease gene.
Many people with autosomal dominant PKD live for several decades without developing symptoms. For this reason, autosomal dominant PKD is often called "adult polycystic kidney disease." Yet, in some cases, cysts may form earlier in life and grow quickly, causing symptoms in childhood.

Picture of polycystic kidney, roughly retains the same shape as the healthy kidney.
The cysts grow out of nephrons, the tiny filtering units inside the kidneys. The cysts eventually separate from the nephrons and continue to enlarge. The kidneys enlarge along with the cysts-which can number in the thousands-while roughly retaining their kidney shape. In fully developed autosomal dominant PKD, a cyst-filled kidney can weigh as much as 20 to 30 pounds. High blood pressure is common and develops in most patients by age 20 or 30.

What are the symptoms of autosomal dominant PKD?

The most common symptoms are pain in the back and the sides (between the ribs and hips), and headaches. The dull pain can be temporary or persistent, mild or severe.
People with autosomal dominant PKD also can experience the following complications:

Urinary tract infections, specifically in the kidney cysts
Hematuria (blood in the urine)
Liver and pancreatic cysts
Abnormal heart valves
High blood pressure
Kidney stones;
Aneurysms (bulges in the walls of blood vessels) in the brain
Diverticulosis (small pouches bulge outward through the colon).

How is autosomal dominant PKD diagnosed?

Autosomal dominant PKD is usually diagnosed by kidney imaging studies. The most common form of diagnostic kidney imaging is ultrasound, but more precise studies, such as computerized tomography (CT) scans or magnetic resonance imaging (MRI) are also widely used. In autosomal dominant PKD, the onset of kidney damage and how quickly the disease progresses can vary. Kidney imaging findings can also vary considerably, depending on a patient's age. Younger patients usually have both fewer and smaller cysts. Doctors have therefore developed specific criteria for diagnosing the disease with kidney imaging findings, depending on patient age. For example, the presence of at least two cysts in each kidney by age 30 in a patient with a family history of the disease can confirm the diagnosis of autosomal dominant PKD. If there is any question about the diagnosis, a family history of autosomal dominant PKD and cysts found in other organs make the diagnosis more likely.
In most cases of autosomal dominant PKD, patients have no symptoms and their physical condition appears normal for many years, so the disease can go unnoticed. Physical checkups and blood and urine tests may not lead to early diagnosis. Because of the slow, undetected progression of cyst growth, some people live for many years without knowing they have autosomal dominant PKD.
Once cysts have grown to about one-half inch, however, diagnosis is possible with imaging technology. Ultrasound, which passes sound waves through the body to create a picture of the kidneys, is used most often. Ultrasound imaging does not use any injected dyes or radiation and is safe for all patients, including pregnant women. It can also detect cysts in the kidneys of a fetus, but large cyst growth this early in life is uncommon in autosomal dominant PKD.
More powerful and expensive imaging procedures such as CT scans and MRI also can detect cysts. Recently, MRI has been used to measure kidney and cyst volume and monitor kidney and cyst growth, which may serve as a way to track progression of the disease.
Diagnosis can also be made with a genetic test that detects mutations in the autosomal dominant PKD genes, called PKD1 and PKD2. Although this test can detect the presence of the autosomal dominant PKD mutations before large cysts develop, its usefulness is limited by two factors: detection of a disease gene cannot predict the onset of symptoms or ultimate severity of the disease, and if a disease gene is detected, no specific prevention or cure for the disease exists. However, a young person who knows of a PKD gene mutation may be able to forestall the loss of kidney function through diet and blood pressure control. The genetic test may also be used to determine whether a young member of a PKD family can safely donate a kidney to a family member with the disease. Individuals with a family history of PKD who are of childbearing age might also want to know whether they have the potential of passing a PKD gene to a child. Anyone considering genetic testing should receive counseling to understand all the implications of the test.

How is autosomal dominant PKD treated?

Although a cure for autosomal dominant PKD is not available, treatment can ease symptoms and prolong life.
Pain. Pain in the area of the kidneys can be caused by cyst infection, bleeding into cysts, kidney stone, or stretching of the fibrous tissue around the kidney with cyst growth. A doctor will first evaluate which of these causes are contributing to the pain to guide treatment. If it is determined to be chronic pain due to cyst expansion, the doctor may initially suggest over-the-counter pain medications, such as aspirin or acetaminophen (Tylenol). Consult your doctor before taking any over-the-counter medication because some may be harmful to the kidneys. For most but not all cases of severe pain due to cyst expansion, surgery to shrink cysts can relieve pain in the back and sides. However, surgery provides only temporary relief and does not slow the disease's progression toward kidney failure.
Headaches that are severe or that seem to feel different from other headaches might be caused by aneurysms-blood vessels that balloon out in spots-in the brain. These aneurysms could rupture, which can have severe consequences. Headaches also can be caused by high blood pressure. People with autosomal dominant PKD should see a doctor if they have severe or recurring headaches-even before considering over-the-counter pain medications.
Urinary tract infections. People with autosomal dominant PKD tend to have frequent urinary tract infections, which can be treated with antibiotics. People with the disease should seek treatment for urinary tract infections immediately because infection can spread from the urinary tract to the cysts in the kidneys. Cyst infections are difficult to treat because many antibiotics do not penetrate the cysts.
High blood pressure. Keeping blood pressure under control can slow the effects of autosomal dominant PKD. Lifestyle changes and various medications can lower high blood pressure. Patients should ask their doctors about such treatments. Sometimes proper diet and exercise are enough to keep blood pressure controlled.
End-stage renal disease. After many years, PKD can cause the kidneys to fail. Because kidneys are essential for life, people with ESRD must seek one of two options for replacing kidney functions: dialysis or transplantation. In hemodialysis, blood is circulated into an external filter, where it is cleaned before re-entering the body; in peritoneal dialysis, a fluid is introduced into the abdomen, where it absorbs wastes and is then removed. Transplantation of healthy kidneys into ESRD patients has become a common and successful procedure. Healthy-non-PKD-kidneys transplanted into PKD patients do not develop cysts.

What is autosomal recessive PKD?

Autosomal recessive PKD is caused by a mutation in the autosomal recessive PKD gene, called PKHD1. Other genes for the disease might exist but have not yet been discovered by scientists. We all carry two copies of every gene. Parents who do not have PKD can have a child with the disease if both parents carry one copy of the abnormal gene and both pass that gene copy to their baby. The chance of the child having autosomal recessive PKD when both parents carry the abnormal gene is 25 percent. If only one parent carries the abnormal gene, the baby cannot get autosomal recessive PKD but could ultimately pass the abnormal gene to his or her children.
The signs of autosomal recessive PKD frequently begin before birth, so it is often called "infantile PKD." Children born with autosomal recessive PKD often, but not always, develop kidney failure before reaching adulthood. Severity of the disease varies. Babies with the worst cases die hours or days after birth due to respiratory difficulties or respiratory failure.
Some people with autosomal recessive PKD do not develop symptoms until later in childhood or even adulthood. Liver scarring occurs in all patients with autosomal recessive PKD and tends to become more of a medical concern with increasing age.

What are the symptoms of autosomal recessive PKD?

Children with autosomal recessive PKD experience high blood pressure, urinary tract infections, and frequent urination. The disease usually affects the liver and spleen, resulting in low blood cell counts, varicose veins, and hemorrhoids. Because kidney function is crucial for early physical development, children with autosomal recessive PKD and decreased kidney function are usually smaller than average size. Recent studies suggest that growth problems may be a primary feature of autosomal recessive PKD.

How is autosomal recessive PKD diagnosed?

Ultrasound imaging of the fetus or newborn reveals enlarged kidneys with an abnormal appearance, but large cysts such as those in autosomal dominant PKD are rarely seen. Because autosomal recessive PKD tends to scar the liver, ultrasound imaging of the liver also aids in diagnosis.

How is autosomal recessive PKD treated?

Medicines can control high blood pressure in autosomal recessive PKD, and antibiotics can control urinary tract infections. Eating increased amounts of nutritious food improves growth in children with autosomal recessive PKD. In some cases, growth hormones are used. In response to kidney failure, autosomal recessive PKD patients must receive dialysis or transplantation. If serious liver disease develops, some people can undergo combined liver and kidney transplantation.

What are genetic diseases?

Genes are segments of DNA, the long molecules that reside in each of a person's cells. The genes, through complex processes, build proteins for growth and maintenance of the body. At conception, DNA-or genes-from both parents are passed to the child.
A genetic disease occurs when one or both parents pass abnormal genes to a child at conception. If receiving an abnormal gene from just one parent is enough to produce a disease in the child, the disease is said to have dominant inheritance. If receiving abnormal genes from both parents is needed to produce disease in the child, the disease is said to be recessive. A genetic disease can also occur through a spontaneous mutation.
The chance of acquiring a dominant disease is higher than the chance of acquiring a recessive disease. A child who receives only one gene copy for a recessive disease at conception will not develop the genetic disease-such as autosomal recessive PKD-but could pass the gene to the following generation.

Hope through research

Scientists have begun to identify the processes that trigger formation of PKD cysts. Advances in the field of genetics have increased our understanding of the abnormal genes responsible for autosomal dominant and autosomal recessive PKD. Scientists have located two genes associated with autosomal dominant PKD. The first was located in 1985 on chromosome 16 and labeled PKD1. PKD2 was localized to chromosome 4 in 1993. Within 3 years, scientists had isolated the proteins these two genes produce-polycystin-1 and polycystin-2.
When both the PKD1 and PKD2 genes are normal, the proteins they produce work together to foster normal kidney development and inhibit cyst formation. A mutation in either of the genes can lead to cyst formation, but evidence suggests that disease development also requires other factors, in addition to the mutation in one of the PKD genes.
Genetic analyses of most families with PKD confirm mutations in either the PKD1 or PKD2 gene. In about 10 to 15 percent of cases, however, families with autosomal dominant PKD do not show obvious abnormalities or mutations in the PKD1 and PKD2 genes, using current testing methods.
Researchers have also recently identified the autosomal recessive PKD gene, called PKHD1, on chromosome 6. Genetic testing for autosomal recessive PKD to detect mutations in PKHD1 is now offered by a limited number of molecular genetic diagnostics laboratories in the United States.
Researchers have bred rodents with a genetic disease that parallels both inherited forms of human PKD. Studying these mice will lead to greater understanding of the genetic and nongenetic mechanisms involved in cyst formation. In recent years, researchers have discovered several compounds that appear to inhibit cyst formation in mice with the PKD gene. Some of these compounds are in clinical testing in humans. Scientists hope further testing will lead to safe and effective treatments for humans with the disease.
Recent clinical studies of autosomal dominant PKD are exploring new imaging methods for tracking progression of cystic kidney disease. These methods, using MRI, are helping scientists design better clinical trials for new treatments of autosomal dominant PKD.
People interested in participating in clinical trials of new treatments for PKD can find a list of centers recruiting patients at www.ClinicalTrials.gov.

Polycystic Kidney Disease At A Glance

The two forms of polycystic kidney disease (PKD) are
- autosomal dominant PKD, a form that usually causes symptoms in adulthood
- autosomal recessive PKD, a rare form that usually causes symptoms in infancy and early childhood
The symptoms and signs of PKD include
- pain in the back and lower sides
- headaches
- urinary tract infections
- blood in the urine
- cysts in the kidneys and other organs
Diagnosis of PKD is obtained by
- ultrasound imaging of kidney cysts
- ultrasound imaging of cysts in other organs
- family medical history, including genetic testing
PKD has no cure. Treatments include
- medicine to control high blood pressure
- medicine and surgery to reduce pain
- antibiotics to resolve infections
- dialysis to replace functions of failed kidneys kidney transplantation

SOURCES:
National Institutes of Health
Medicinenet.com.

References: Grantham JJ, Nair V, Winklhoffer F. Cystic diseases of the kidney. In: Brenner BM, ed. Brenner & Rector's The Kidney. Vol. 2. 6th ed. Philadelphia: WB Saunders Company; 2000: 1699-1730.

Mitochondrial Disease

2012-03-17T04:04:00.001-07:00

What is Mitochondrial Myopathies?

Mitochondrial myopathies are a group of neuromuscular diseases caused by damage to the mitochondria-small, energy-producing structures that serve as the cells' "power plants." Nerve cells in the brain and muscles require a great deal of energy, and thus appear to be particularly damaged when mitochondrial dysfunction occurs. Some of the more common mitochondrial myopathies include Kearns-Sayre syndrome, myoclonus epilepsy with ragged-red fibers, and mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes. The symptoms of mitochondrial myopathies include:

muscle weakness or exercise intolerance,
heart failure or rhythm disturbances,
dementia,
movement disorders,
stroke-like episodes,
deafness,
blindness,
droopy eyelids,
limited mobility of the eyes,
vomiting, and
seizures.

The prognosis for these disorders ranges in severity from progressive weakness to death. Most mitochondrial myopathies occur before the age of 20, and often begin with exercise intolerance or muscle weakness. During physical activity, muscles may become easily fatigued or weak. Muscle cramping is rare, but may occur. Nausea, headache, and breathlessness are also associated with these disorders.

Is there any treatment for mitochondrial disease?

Although there is no specific treatment for any of the mitochondrial myopathies, physical therapy may extend the range of movement of muscles and improve dexterity. Vitamin therapies such as riboflavin, coenzyme Q, and carnitine (a specialized amino acid) may provide subjective improvement in fatigue and energy levels in some patients.

What is the prognosis for mitochondrial disease?

The prognosis for patients with mitochondrial myopathies varies greatly, depending largely on the type of disease and the degree of involvement of various organs. These disorders cause progressive weakness and can lead to death.

What research is being done for mitochondrial disease?

The NINDS conducts and supports research on mitochondrial myopathies. The goals of this research are to increase scientific understanding of these disorders and to find ways to effectively treat, prevent, or potentially cure them.
Select this link to view a list of studies currently seeking patients.

Organizations

Muscular Dystrophy Association
3300 East Sunrise Drive
Tucson, AZ 85718-3208
mda@mdausa.org
http://www.mda.org
Tel: 520-529-2000
800-344-4863
Fax: 520-529-5300
United Mitochondrial Disease Foundation
8085 Saltsburg Road Suite 201
Pittsburgh, PA 15239
info@umdf.org
http://www.umdf.org
Tel: 412-793-8077
Fax: 412-793-6477
National Organization for Rare Disorders (NORD)
P.O. Box 1968 (55 Kenosia Avenue)
Danbury, CT 06813-1968
orphan@rarediseases.org
http://www.rarediseases.org
Tel: 203-744-0100
Voice Mail 800-999-NORD (6673)
Fax: 203-798-2291

SOURCES: National Institute of Neurological Disorders and Stroke

Medicinenet.com.

Fabry Disease

2012-03-17T04:03:00.001-07:00

What is Fabry disease?

Fabry disease is caused by the lack of or faulty enzyme needed to metabolize lipids, fat-like substances that include oils, waxes, and fatty acids. The enzyme is known as ceramide trihexosidase, also called alpha-galactosidase-A. A mutation in the gene that controls this enzyme causes insufficient breakdown of lipids, which build up to harmful levels in the eyes, kidneys, autonomic nervous system, and cardiovascular system. Since the gene that is altered is carried on a mother's X chromosome, her sons have a 50 percent chance of inheriting the disorder and her daughters have a 50 percent chance of being a carrier.

What are the symptoms of Fabry disease?

Some women who carry the genetic mutation may have symptoms of the disease. Symptoms usually begin during childhood or adolescence and include:

burning sensations in the hands that gets worse with exercise and hot weather, and
small, raised reddish-purple blemishes on the skin.

Some boys will also have eye manifestations, especially cloudiness of the cornea. Lipid storage may lead to impaired arterial circulation and increased risk of heart attack or stroke. The heart may also become enlarged and the kidneys may become progressively involved.
Other symptoms include:

decreased sweating,
fever, and
gastrointestinal difficulties, particularly after eating.

Fabry disease is one of several lipid storage disorders.

Is there any treatment for Fabry disease?

Enzyme replacement may be effective in slowing the progression of the disease. The pain in the hands and feet usually responds to anticonvulsants such as phenytoin (Dilantin) and carbamazepine (Tegretol, Tegretol XR , Equetro, Carbatrol). Gastrointestinal hyperactivity may be treated with metoclopramide (Reglan, Octamide, Maxolon). Some individuals may require dialysis or kidney transplantation.

What is the prognosis for Fabry disease?

Patients with Fabry disease often survive into adulthood but are at increase risk of strokes, heart attack and heart disease, and kidney failure.

What research is being done on Fabry disease?

The National Institute of Neurological Disorders and Stroke (NINDS), a component of the National Institutes of Health, conducts and supports research to find ways to treat and prevent lipid storage diseases such as Fabry disease. This research includes clinical studies by the NINDS Developmental and Metabolic Neurology Branch:http://www.ninds.nih.gov/find_people/labs/61.htm.

For more information

Fabry Support & Information Group
108 NE 2nd Street, Ste. C
P.O. Box 510 Concordia, MO 64020-0510
info@fabry.org
http://www.fabry.org
Tel: 660-463-1355
Fax: 660-463-1356
National Tay-Sachs and Allied Diseases Association
2001 Beacon Street Suite 204
Brighton, MA 02135
info@ntsad.org
http://www.ntsad.org
Tel: 617-277-4463 800-90-NTSAD (906-8723)
Fax: 617-277-0134
National Organization for Rare Disorders (NORD)
P.O. Box 1968 (55 Kenosia Avenue)
Danbury, CT 06813-1968
orphan@rarediseases.org
http://www.rarediseases.org
Tel: 203-744-0100
Voice Mail 800-999-NORD (6673)
Fax: 203-798-2291

SOURCES: National Institute of Neurological Disorders and Stroke

Medicinenet.com.

Heart Attacks in Women

2012-03-17T04:02:00.002-07:00

One woman's heart attack story

In 1991, I went to the ER with chest pains twice in one week. They said it was ulcers (bleeding in the stomach). Then the pain became very intense. Again, the ER said there was nothing they could do. I refused to leave and was admitted for observation. Later, the doctor on duty saw my EKG and asked, "Where's the 34-year-old who had the massive heart attack?" I had emergency surgery. But the damage was done; only part of my heart muscle functions. I had to quit a job I loved, and my life is completely changed. They thought I was too young to have a heart attack.

What is heart disease?

Heart disease includes a number of problems affecting the heart and the blood vessels in the heart. Types of heart disease include:
Coronary artery disease (CAD) is the most common type and is the leading cause of heart attacks. When you have CAD, your arteries become hard and narrow. Blood has a hard time getting to the heart, so the heart does not get all the blood it needs. CAD can lead to:

Angina (an-JEYE-nuh). Angina is chest pain or discomfort that happens when the heart does not get enough blood. It may feel like a pressing or squeezing pain, often in the chest, but sometimes the pain is in the shoulders, arms, neck, jaw, or back. It can also feel like indigestion (upset stomach). Angina is not a heart attack, but having angina means you are more likely to have a heart attack.
Heart attack. A heart attack occurs when an artery is severely or completely blocked, and the heart does not get the blood it needs for more than 20 minutes.

Heart failure occurs when the heart is not able to pump blood through the body as well as it should. This means that other organs, which normally get blood from the heart, do not get enough blood. It does not mean that the heart stops. Signs of heart failure include:

Shortness of breath (feeling like you can't get enough air)
Swelling in feet, ankles, and legs
Extreme tiredness

Heart arrhythmias (uh-RITH-mee-uhz) are changes in the beat of the heart. Most people have felt dizzy, faint, out of breath or had chest pains at one time. These changes in heartbeat are harmless for most people. As you get older, you are more likely to have arrhythmias. Don't panic if you have a few flutters or if your heart races once in a while. If you have flutters and other symptoms such as dizziness or shortness of breath, call 911 right away.

Do women need to worry about heart disease?

Yes. Among all U.S. women who die each year, one in four dies of heart disease. In 2004, nearly 60 percent more women died of cardiovascular disease (both heart disease and stroke) than from all cancers combined. The older a woman gets, the more likely she is to get heart disease. But women of all ages should be concerned about heart disease. All women should take steps to prevent heart disease.
Both men and women have heart attacks, but more women who have heart attacks die from them. Treatments can limit heart damage but they must be given as soon as possible after a heart attack starts. Ideally, treatment should start within one hour of the first symptoms.
If you think you're having a heart attack, call 911 right away. Tell the operator your symptoms and that you think you're having a heart attack.

Do women of color need to worry about heart disease?

Yes. African American and Hispanic American/Latina women should be concerned about getting heart disease because they tend to have more risk factors than white women. These risk factors include obesity, lack of physical activity, high blood pressure, and diabetes. If you're a woman of color, take steps to reduce your risk factors.

What can I do to prevent heart disease?

You can reduce your chances of getting heart disease by taking these steps:
Know your blood pressure. Years of high blood pressure can lead to heart disease. People with high blood pressure often have no symptoms, so have your blood pressure checked every 1 to 2 years and get treatment if you need it.
Don't smoke. If you smoke, try to quit. If you're having trouble quitting, there are products and programs that can help:

Nicotine patches and gums
Support groups
Programs to help you stop smoking

Ask your doctor or nurse for help to provide information and therapies to help quit smoking.
Get tested for diabetes. People with diabetes have high blood glucose (often called blood sugar). People with high blood glucose often have no symptoms, so have your blood glucose checked regularly. Having diabetes raises your chances of getting heart disease. If you have diabetes, your doctor will decide if you need diabetes pills or insulin shots. Your doctor can also help you make a healthy eating and exercise plan.
Get your cholesterol and triglyceride levels tested. High blood cholesterol (koh-LESS-tur-ol) can clog your arteries and keep your heart from getting the blood it needs. This can cause a heart attack. Triglycerides (treye-GLIH-suh-ryds) are a form of fat in your blood stream. High levels of triglycerides are linked to heart disease in some people. People with high blood cholesterol or high blood triglycerides often have no symptoms, so have both levels checked regularly. If your levels are high, talk to your doctor about what you can do to lower them. You may be able to lower your both levels by eating better and exercising more. Your doctor may prescribe medication to help lower your cholesterol.
Maintain a healthy weight. Being overweight raises your risk for heart disease. Calculate your Body Mass Index (BMI) to see if you are at a healthy weight. Healthy food choices and physical activity are important to staying at a healthy weight:

Start by adding more fruits, vegetables, and whole grains to your diet.
Each week, aim to get at least 2 hours and 30 minutes of moderate physical activity, 1 hour and 15 minutes of vigorous physical activity, or a combination of moderate and vigorous activity.

If you drink alcohol, limit it to no more than one drink (one 12 ounce beer, one 5 ounce glass of wine, or one 1.5 ounce shot of hard liquor) a day.
Find healthy ways to cope with stress. Lower your stress level by talking to your friends, exercising, or writing in a journal.
Take action to reduce heart disease risk:

Be physically active
Don't smoke
Eat healthy
Maintain a normal weight
Know your numbers (blood pressure, cholesterol, and triglycerides)

What does high blood pressure have to do with heart disease?

Blood pressure is the force your blood makes against the walls of your arteries. The pressure is highest when your heart pumps blood into your arteries – when it beats. It is lowest between heart beats, when your heart relaxes. A doctor or nurse will write down your blood pressure as the higher number over the lower number. For instance, you could have a blood pressure of 110/70 (read as "110 over 70"). A blood pressure reading below 120/80 is usually considered normal. Very low blood pressure (lower than 90/60) can sometimes be a cause of concern and should be checked out by a doctor.
High blood pressure, or hypertension, is a blood pressure reading of 140/90 or higher. Years of high blood pressure can damage artery walls, causing them to become stiff and narrow. This includes the arteries carrying blood to the heart. As a result, your heart cannot get the blood it needs to work well. This can cause a heart attack.
A blood pressure reading of 120/80 to 139/89 is considered prehypertension. This means that you don't have high blood pressure now but are likely to develop it in the future.

How can I lower my blood pressure?

If you have hypertension or prehypertension, you may be able to lower your
blood pressure by:

losing weight if you are overweight or obese
getting at least 2 hours and 30 minutes of moderate physical activity or 1 hour and 15 minutes of vigorous activity each week.
limiting alcohol to one drink per day
quitting smoking if you smoke
reducing stress
following the DASH (Dietary Approaches to Stop Hypertension) Eating Plan, which includes cutting down on salt and sodium and eating healthy foods, such as fruits, vegetables, and low-fat dairy products

If lifestyle changes do not lower your blood pressure, your doctor may prescribe medicine.

What does high cholesterol have to do with heart disease?

Cholesterol is a waxy substance found in cells in all parts of the body. When there is too much cholesterol in your blood, cholesterol can build up on the walls of your arteries and cause blood clots. Cholesterol can clog your arteries and keep your heart from getting the blood it needs. This can cause a heart attack.
There are two types of cholesterol:

Low-density lipoprotein (LDL) is often called the "bad" type of cholesterol because it can clog the arteries that carry blood to your heart. For LDL, lower numbers are better.
High-density lipoprotein (HDL) is known as "good" cholesterol because it takes the bad cholesterol out of your blood and keeps it from building up in your arteries. For HDL, higher numbers are better.

All women age 20 and older should have their blood cholesterol and triglyceride levels checked at least once every 5 years.

What do my cholesterol and triglyceride numbers mean?

Total cholesterol level - Lower is better. Less than 200 mg/dL is best.
Total Cholesterol Level	Category
Less than 200 mg/dl	Desirable
200 - 239 mg/dl	Borderline high
240 mg/dl	High

LDL (bad) cholesterol - Lower is better. Less than 100 mg/dL is best.
LDL Cholesterol Level	Category
Less than 100 mg/dl	Optimal
100 - 129 mg/dl	Near optimal/above optimal
130 - 159 mg/dl	Borderline high
160 - 189 mg/dl	High
190 mg/dl and above	Very High

HDL (good) cholesterol - Higher is better. More than 60 mg/dL is best.
Triglyceride levels - Lower is better. Less than 150mg/dL is best.

How can I lower my cholesterol?

You can lower your cholesterol by taking these steps:
Maintain a healthy weight. If you are overweight, losing weight can help lower your total cholesterol and LDL ("bad cholesterol") levels. Calculate your Body Mass Index (BMI) to see if you are at a healthy weight. If not, try making small changes like eating an apple instead of potato chips, taking the stairs instead of the elevator, or parking farther away from the entrance to your office, the grocery store, or the mall. (But be sure to park in a safe, well-lit spot.)
Eat better. Eat foods low in saturated fats, trans fats, and cholesterol.
Eat more:

Fish, poultry (chicken, turkey--breast meat or drumstick is best), and lean meats (round, sirloin, tenderloin). Broil, bake, roast, or poach foods. Remove the fat and skin before eating.
Skim (fat-free) or low-fat (1%) milk and cheeses, and low-fat or nonfat yogurt
Fruits and vegetables (try for 5 a day)
Cereals, breads, rice, and pasta made from whole grains (such as "whole-wheat" or "whole-grain" bread and pasta, rye bread, brown rice, and oatmeal)

Eat less:

Organ meats (liver, kidney, brains)
Egg yolks
Fats (butter, lard) and oils
Packaged and processed foods

There are two diets that may help lower your cholesterol:

Heart Healthy Diet
Therapeutic Lifestyles Changes (TLC) Diet

Get moving. Exercise can help lower LDL ("bad cholesterol") and raise HDL ("good cholesterol"). Exercise at a moderate intensity for at least 2 hours and 30 minutes each week, or get 1 hour and 15 minutes of vigorous intensity physical activity each week.

Take your medicine. If your doctor has prescribed medicine to lower your cholesterol, take it exactly as you have been told to.

How do I know if I have heart disease?

Heart disease often has no symptoms. But, there are some signs to watch for. Chest or arm pain or discomfort can be a symptom of heart disease and a warning sign of a heart attack. Shortness of breath (feeling like you can't get enough air), dizziness, nausea (feeling sick to your stomach), abnormal heartbeats, or feeling very tired also are signs. Talk with your doctor if you're having any of these symptoms. Tell your doctor that you are concerned about your heart. Your doctor will take a medical history, do a physical exam, and may order tests.

What are the signs and symptoms of a heart attack?

For both women and men, the most common sign of a heart attack is:

Pain or discomfort in the center of the chest. The pain or discomfort can be mild or strong. It can last more than a few minutes, or it can go away and come back.

Other common signs of a heart attack include:

Pain or discomfort in one or both arms, back, neck, jaw, or stomach
Shortness of breath (feeling like you can't get enough air). The shortness of breath often occurs before or along with the chest pain or discomfort.
Nausea (feeling sick to your stomach) or vomiting
Feeling faint or woozy
Breaking out in a cold sweat

Women are more likely than men to have these other common signs of a heart attack, particularly shortness of breath, nausea or vomiting, and pain in the back, neck, or jaw. Women are also more likely to have less common signs of a heart attack, including:

Heartburn
Loss of appetite
Feeling tired or weak
Coughing
Heart flutters

Sometimes the signs of a heart attack happen suddenly, but they can also develop slowly, over hours, days, and even weeks before a heart attack occurs.
The more heart attack signs that you have, the more likely it is that you are having a heart attack. Also, if you've already had a heart attack, your symptoms may not be the same for another one. Even if you're not sure you're having a heart attack, you should still have it checked out.
If you think you, or someone else, may be having a heart attack, wait no more than a few minutes - five at most - before calling 911.

One of my family members had a heart attack. Does that mean I'll have one too?

If your dad or brother had a heart attack before age 55, or if your mom or sister had one before age 65, you're more likely to develop heart disease. This does not mean you will have a heart attack. It means you should take extra good care of your heart to keep it healthy.

Sometimes my heart beats really fast and other times it feels like my heart skips a beat. Am I having a heart attack?

Most people have changes in their heartbeat from time to time. These changes in heartbeat are, for most people, harmless. As you get older, you're more likely to have heartbeats that feel different. Don't panic if you have a few flutters or if your heart races once in a while. If you have flutters and other symptoms such as dizziness or shortness of breath (feeling like you can't get enough air), call 911.

Should I take a daily aspirin to prevent heart attack?

Aspirin may be helpful for women at high risk, such as women who have already had a heart attack. Aspirin can have serious side effects and may be harmful when mixed with certain medicines. If you're thinking about taking aspirin, talk to your doctor first. If your doctor thinks aspirin is a good choice for you, be sure to take it exactly as your doctor tells you to.

Does taking birth control pills increase my risk for heart disease?

Taking birth control pills is generally safe for young, healthy women if they do not smoke. But birth control pills can pose heart disease risks for some women, especially women older than 35; women with high blood pressure, diabetes, or high cholesterol; and women who smoke. Talk with your doctor if you have questions about the pill.
If you're taking birth control pills, watch for signs of trouble, including:

Eye problems such as blurred or double vision
Pain in the upper body or arm
Bad headaches
Problems breathing
Spitting up blood
Swelling or pain in the leg
Yellowing of the skin or eyes
Breast lumps
Unusual (not normal) heavy vaginal bleeding

If you have any of these symptoms, call 911.

Does using the birth control patch increase my risk for heart disease?

The patch is generally safe for young, healthy women. The patch can pose heart disease risks for some women, especially women older than 35; women with high blood pressure, diabetes, or high cholesterol; and women who smoke.
Recent studies show that women who use the patch may be exposed to more estrogen than women who use the birth control pill. Estrogen is the female hormone in birth control pills and the patch that keeps you from getting pregnant. Research is underway to see if the risk for blood clots is higher in patch users. Blood clots can lead to heart attack or stroke. Talk with your doctor if you have questions about the patch.
If you're using the patch, watch for signs of trouble, including:

Eye problems such as blurred or double vision
Pain in the upper body or arm
Bad headaches
Problems breathing
Spitting up blood
Swelling or pain in the leg
Yellowing of the skin or eyes
Breast lumps
Unusual (not normal) heavy bleeding from your vagina

If you have any of these symptoms, call 911.

Does menopausal hormone therapy (HT, HRT, ET) increase a woman's risk for heart disease?

Menopausal hormone therapy (MHT) can help with some symptoms of menopause, including hot flashes, vaginal dryness, mood swings, and bone loss, but there are risks, too. For some women, taking hormones can increase their chances of having a heart attack or stroke. If you decide to use hormones, use them at the lowest dose that helps for the shortest time needed. Talk with your doctor if you have questions about MHT.

For more information on heart disease in women

For more information on heart disease, please call womenshealth.gov at 1-800-994-9662 or contact the following organizations:
National Heart, Lung, and Blood Institute (NHLBI)
Phone Number(s): (301) 592-8573
Internet Address:
www.nhlbi.nih.gov/index.htm
National Cholesterol Education Program
National Heart, Lung, and Blood Institute (NHLBI)
Internet Address:
www.nhlbi.nih.gov/about/ncep
National High Blood Pressure Education Program
National Heart, Lung, and Blood Institute (NHLBI)
Internet Address:
www.nhlbi.nih.gov/about/nhbpep/index.htm
Act In Time to Heart Attack Signs Campaign
National Heart Attack Alert Program
National Heart, Lung, and Blood Institute (NHLBI)
Phone Number(s): (301) 592-8573
Internet Address:
www.nhlbi.nih.gov/actintime
The Heart Truth
National Awareness Campaign for Women about Heart Disease
National Heart, Lung, and Blood Institute (NHLBI)
Internet Address:
www.nhlbi.nih.gov/health/hearttruth/index.htm
American Heart Association
Phone Number(s): (800) 242-8721
Internet Address:
www.americanheart.org
WomenHeart
Phone Number(s): (202) 728-7199
Internet Address:
www.womenheart.org
Reviewed by: Patrice Desvigne-Nickens, M.D. Program Director Heart Failure & Arrhythmias Branch Division of Cardiovascular Diseases National Heart, Lung, and Blood Institute

SOURCES:
womenshealth.gov. Heart Disease.
<http://www.womenshealth.gov/faq/heart-disease.cfm>

Medicinenet.com.

Sickle Cell Disease (Sickle Cell Anemia)

2012-03-17T03:59:00.001-07:00

What is sickle cell anemia?

Sickle cell anemia (sickle cell disease) is a disorder of the blood caused by an inherited abnormal hemoglobin (an oxygen-carrying protein within the red blood cells). The abnormal hemoglobin causes distorted (sickled) red blood cells. The sickled red blood cells are fragile and prone to rupture. When the number of red blood cells decreases from rupture (hemolysis), anemia is the result. This condition is referred to as sickle cell anemia. The irregular sickled cells can also block blood vessels causing tissue and organ damage and pain.
Sickle cell anemia is one of the most common inherited blood anemias. The disease primarily affects Africans and African Americans. It is estimated that in the United States, some 50,000 African Americans are afflicted with the most severe form of sickle cell anemia. Overall, current estimates are that one in 1,875 U.S. African American is affected with sickle cell anemia.
How is sickle cell anemia inherited?
Sickle cell anemia is inherited as an autosomal (meaning that the gene is not linked to a sex chromosome) recessive condition whereas sickle cell trait is inherited as an autosomal dominant trait. This means that the gene can be passed on from a parent carrying it to male and female children. In order for sickle cell anemia to occur, a sickle cell gene must be inherited from both the mother and the father, so that the child has two sickle cell genes.
The inheritance of just one sickle gene is called sickle cell trait or the "carrier" state. Sickle cell trait does not cause sickle cell anemia. Persons with sickle cell trait usually do not have many symptoms of disease and have normal hospitalization rates and life expectancies. Sickle cell trait is present in some two million blacks in the United States (8% of the U.S. black population at birth). When two carriers of sickle cell trait mate, their offspring have a one in four chance of having sickle cell anemia. (In some parts of Africa, one in five persons is a carrier for sickle cell trait.)

What conditions promote the sickling (distortion) of the red blood cells in sickle cell anemia?
Sickling of the red blood cells in patients with sickle cell anemia results in cells of abnormal shape and flexibility. The sickling is promoted by conditions which are associated with low oxygen levels, increased acidity, or low volume (dehydration) of the blood. These conditions can occur as a result of injury to the body's tissues, dehydrating states, or anesthesia.
Even certain organs are predisposed to lower oxygen levels or acidity, such as when blood moves slowly through the spleen, liver, or kidney. Also, organs with particularly high metabolism rates (such as the brain, muscles, and the placenta in a pregnant woman with sickle cell anemia) promote sickling by extracting more oxygen from the blood. These conditions make these organs susceptible to injury from sickle cell anemia.
How is sickle cell anemia diagnosed?
Sickle cell anemia is suggested when the abnormal sickle-shaped cells in the blood are identified under a microscope. Testing is typically performed on a smear of blood using a special low-oxygen preparation. This is referred to as a sickle prep. Other prep tests can also be used to detect the abnormal hemoglobin S, including solubility tests performed on tubes of blood solutions. The disease can be confirmed by specifically quantifying the types of hemoglobin present using a hemoglobin electrophoresis test.
Prenatal diagnosis (before birth) of sickle cell anemia is possible using amniocentesis or chorionic villus sampling. The sample obtained is then tested for DNA analysis of the fetal cells.
The hemoglobin electrophoresis test precisely identifies the hemoglobins in the blood by separating them. The separation of the different hemoglobins is possible because of the unique electrical charges they each have on their protein surfaces, causing them each to move characteristically in an electrical field as tested in the laboratory.
What are the symptoms and treatments of sickle cell anemia?
Virtually all of the major symptoms of sickle cell anemia are the direct result of the abnormally shaped, sickled red blood cells blocking the flow of blood that circulates through the tissues of the body. The tissues with impaired circulation suffer damage from lack of oxygen. Damage to tissues and organs of the body can cause severe disability in patients with sickle cell anemia. The patients endure episodes of intermittent "crises" of variable frequency and severity, depending on the degree of organ involvement.
The major features of sickle cell anemia include:

Fatigue and Anemia
Pain Crises
Dactylitis (swelling and inflammation of the hands and/or feet) and Arthritis
Bacterial Infections
Splenic Sequestration (sudden pooling of blood in the spleen) and Liver Congestion
Lung and Heart Injury
Leg Ulcers
Aseptic Necrosis and Bone Infarcts (death of portions of bone)
Eye Damage
Other Features

Some features of sickle cell anemia, such as fatigue, anemia, pain crises, and bone infarcts can occur at any age. Many features typically occur in certain age groups.
Sickle cell anemia usually first presents symptoms in the first year of life. Infants and younger children can suffer with fever, abdominal pain, pneumococcal bacterial infections, painful swellings of the hands and feet (dactylitis), and splenic sequestration. Adolescents and young adults more commonly develop leg ulcers, aseptic necrosis, and eye damage. Symptoms in adult typically are intermittent pain episodes due to injury of bone, muscle, or internal organs.
Affected infants do not develop symptoms in the first few months of life because the hemoglobin produced by the developing fetus (fetal hemoglobin) protects the red blood cells from sickling. This fetal hemoglobin is absent in the red blood cells that are produced after birth so that by 5 months of age, the sickling of the red blood cells is prominent and symptoms begin.
The treatment of sickle cell anemia is designed according to which of the individual features of the illness are present. In general treatment is directed at the management and prevention of the acute manifestations as well as therapies directed toward blocking the red blood cells from stacking together. There is no single remedy to reverse the anemia. It is, therefore, important that family members have an optimal understanding of the illness and that communication with the doctors and medical personnel be maintained.
Fatigue and Anemia
Fatigue is a common symptom in persons with sickle cell anemia. Sickle cell anemia causes a chronic form of anemia which can lead to fatigue. The sickled red blood cells are prone to breakage (rupture) which causes a much shorter life span of these cells (the normal life span of a red blood cell is 120 days). These sickled red blood cells are easily detected with a microscope examination of a smear of blood on a glass slide.
Typically, the site of red blood cell production (bone marrow) works overtime to produce these cells rapidly, attempting to compensate for their destruction in the circulation. Occasionally, the bone marrow suddenly stops producing the red blood cells which causes a very severe form of anemia (aplastic crises). Aplastic crises can be promoted by infections that otherwise would seem less significant, including viruses of the stomach and bowels and the flu (influenza).
The anemia of sickle cell anemia tends to stabilize without specific treatments. The degree of anemia is defined by measurement of the blood hemoglobin level. Hemoglobin is the protein molecule in red blood cells which carries oxygen from the lungs to the body's tissues and returns carbon dioxide from the tissues to the lungs. Blood hemoglobin levels in persons with sickle cell anemia are generally between 6 to 8 gms/dl (normal levels are above 11 gms/dl). Occasionally, there can be a severe drop in hemoglobin requiring a blood transfusion to correct the anemia (such as in patients suffering splenic sequestration). Blood transfusion is usually reserved for those patients with other complications, including pneumonia, lung infarction, stroke, severe leg ulceration, or late pregnancy. (Among the risks of blood transfusion are hepatitis, infection, immune reaction, and injury to body tissues from iron overload.) Transfusions are also given to patients to prepare them for surgical procedures. Folic acid is given as a supplement.
Pain Crises
Pain crises in persons with sickle cell anemia are intermittent painful episodes that are the result of inadequate blood supply to body tissues. The impaired circulation is caused by the blockage of various blood vessels from the sickling of red blood cells. The sickled red blood cells slow or completely impede the normal flow of blood through the tissues. This leads to excruciating pain requiring hospitalization and narcotic medication for relief. The pain typically is throbbing and can change its location from one body area to another. Bone is frequently affected. Pain in the abdomen with tenderness is common and can mimic appendicitis. Fever frequently is associated with the pain crises.
A pain crisis can be promoted by preceding dehydration, infection, injury, cold exposure, emotional stress, or strenuous exercise. As a prevention measure, persons with sickle cell anemia should avoid extremes of heat and cold.
Pain crises require medications for pain and increased fluid intake. Dehydration must be prevented to avoid further injury to the tissues and intravenous fluids can be necessary. Along with the fluids clotrimazole and magnesium are often given. Other modalities, such as biofeedback, self-hypnosis, and/or electrical nerve stimulation may be helpful.
Hydroxyurea is a medication that is currently being used in adults and children with severe pain from sickle cell anemia. It is also considered for those with recurrent strokes and frequent transfusions. This drug acts by increasing the amount of fetal hemoglobin in the blood (this form of hemoglobin is resistant to sickling of the red blood cells). The response to hydroxyurea is variable and unpredictable from patient to patient. Hydroxyurea can be toxic to the bone marrow.
Dactylitis and Arthritis
Swelling and inflammation of the hands and/or feet is often an early sign of sickle cell anemia. The swelling involves entire fingers and/or toes and is called dactylitis. Dactylitis is caused by injury to the bones of the affected digits by repeated episodes of inadequate blood circulation. Dactylitis generally occurs in children with sickle cell anemia from age 6 months to 8 years.
Joint inflammation (arthritis) with pain, swelling, tenderness, and limited range of motion can accompany the dactylitis. Sometimes, not only the joints of the hands or feet are affected, but also a knee or an elbow.
The inflammation from dactylitis and arthritis can be reduced by anti-inflammation medications, such as ibuprofen and aspirin.
Bacterial Infection
Lung infection (pneumonia) is extremely common in children with sickle cell anemia and is also the most common reason for hospitalization. Pneumonia can be slow to respond to antibiotics. The type of bacteria that is frequently the cause of pneumonia is called pneumococcus bacteria. (This is, in part, due to the increased susceptibility to this particular bacteria when the spleen is poorly functioning.) Vaccination against pneumococcal infection is generally recommended.
Children with sickle cell anemia are also at risk for infection of the brain and spinal fluid (meningitis). Bacteria that are frequent causes of this infection include the Pneumococcus and Haemophilus bacteria.
Furthermore, children with sickle cell anemia are at risk for an unusual form of bone infection (osteomyelitis). The infection is typically from a bacteria called Salmonella.
Bacterial infections can be serious and even overwhelming for patients with sickle cell anemia. Early detection and antibiotic treatment are the keys to minimizing complications. Any child with known sickle cell anemia must be evaluated by medical professionals when fever or other signs of infection (such as unexplained pain or cough) appear.
Splenic Sequestration and Liver Congestion
It has been demonstrated that the liver, and especially the spleen, are organs that are very active in removing sickled red blood cells from the circulation of persons with sickle cell anemia. This process can accelerate suddenly. Sudden pooling of blood in the spleen is referred to as splenic sequestration.
Splenic sequestration can cause very severe anemia and even result in death.
The spleen is commonly enlarged (splenomegaly) in younger children with sickle cell anemia. As the spleen is repeatedly injured by damage from impaired blood supply, it gradually shrinks with scarring. Impairment of the normal function of the spleen increases the tendency to become infected with bacteria.
Sudden pooling of blood in the spleen (splenic sequestration) can result in a very severe anemia and death. These patients can develop shock and lose consciousness. Transfusion of blood and fluids can be critical if this occurs.
Liver enlargement (hepatomegaly) occurs as it becomes congested with red blood cells as well. The liver is often firm and can become tender. Impaired liver function can result in yellowing of the eyes (jaundice). The gallbladder, which drains bile from the liver, can fill with gallstones. Inflammation of the gallbladder (cholecystitis) can cause nausea and vomiting and require its removal.
Lung and Heart Injury
Aside from lung infection (pneumonia), the lungs of children with sickle cell anemia can also be injured by inadequate circulation of blood which causes areas of tissue death. This lung damage can be difficult to distinguish from pneumonia. These localized areas of lung tissue damage are referred to as pulmonary infarcts. Pulmonary infarcts often require a special x-ray test using a dye injected into the affected areas (angiogram) for diagnosis. Repeated pulmonary infarcts can lead to scarring of the lungs of children with sickle cell anemia by the time they reach adolescence.
The heart is frequently enlarged in children with sickle cell anemia. Rapid heart rates and murmurs are common. The heart muscle can also be injured by infarcts and iron depositing in the muscle as it leaks from the ruptured red blood cells.
Injuries to the lungs or heart are treated according to the specific type of damage and the degree of impairment of organ function. Supplementary oxygen can be required. Infections of the lungs require aggressive antibiotics. Transfusions can sometimes help prevent further damage to the lung tissue. Heart failure can require chronic heart medications to assist the heart in pumping blood to the body.
Leg Ulcers
The legs of patients with sickle cell anemia are susceptible to skin breakdown and ulceration. This seems to be a result of the stagnant blood flow caused by the sickled red blood cells. Injury to the skin of the legs or ankles can promote skin damage and ulceration.
Leg ulcers most commonly occur in adults and usually form over the ankles and sides of the lower legs. The ulcers can become severe, even encircling the leg, and are prone to infection.
Leg ulcers can become chronic and resistant to many treatments. Oral antibiotics and topical creams are often used. Elevation of the leg, careful dressing changes, and other topical therapies can be helpful. Some ulcers can be so resistant that skin grafting is recommended, though this is not without the possibility of poor healing.
Aseptic Necrosis and Bone Infarcts
Inadequate circulation of the blood, which is characteristic of sickle cell anemia, also causes areas of death of bone tissue (bone infarction). Aseptic necrosis, or localized bone death, is a result of inadequate oxygen supply to the bone. Aseptic necrosis is also referred to as osteonecrosis.
While virtually any bone can be affected, the most common are the bones of the thighs, legs, and arms. The result can permanently damage or deform the hips, shoulders, or knees. Pain, tenderness, and disability frequently are signs of aseptic necrosis. Painful bone infarcts can be relieved by rest and pain medications.
Aseptic necrosis can permanently damage large joints (such as the hips or shoulders). Local pain can be relieved and worsening of the condition can be prevented by avoiding weight bearing. With more severe damage, total joint replacement may be needed to restore function.
Eye Damage
The critical area of the eye that normally senses light is called the retina. The retina is in the back of the eye and is nourished by many tiny blood vessels. Impairment of the circulation from the sickling of red blood cells results in damage to the retina (retinopathy). The result can be partial or complete blindness.
Bleeding can also occur within the eye (retinal hemorrhage) and retinal detachment can result. Retinal detachment can lead to blindness.
Once blindness occurs, it is usually permanent. Preventative measures, such as laser treatments, can be used if bleeding into the eye and retinal detachment are detected early.
Other Features
Additional features of sickle cell anemia include weakening of bones from osteoporosis, kidney damage and infection, and nervous system damage. Osteoporosis can lead to severe pain in the back and deformity from collapse of the bony building blocks (vertebrae) of the spine. Kidney damage can lead to poor kidney function with a resulting imbalance of blood sodium and acidity as well as bleeding into the urine. Kidney infection can cause pelvic pain and require hospitalization with antibiotic treatment. Injury to the nervous system can result from meningitis or sickle cell anemia itself. Poor blood circulation in the brain can cause stroke, convulsions, and coma.
Damage to the brain from stroke can cause permanent loss of function to areas of the body. Transfusion of blood and fluids intravenously can be critical. Medications to reduce the chance of seizures are sometimes added. If stroke results in long-term impairment of function, physical therapy, speech therapy, and occupational therapy can be helpful.
Priapism, an abnormally persistent erection of the penis in the absence of sexual desire, can occur in persons with sickle cell anemia. Priapism can lead to impotence.
What is the outlook (prognosis) for patients with sickle cell anemia?
The life expectancy of persons with sickle cell anemia is reduced. Some patients, however, can remain without symptoms for years, while others do not survive infancy or early childhood. Nevertheless, with optimal management patients can now survive beyond the fourth decade.
Most patients suffer intermittent pain crises, fatigue, bacterial infections, and progressive tissue and organ damage. Impaired growth and development is the end result of the physical and emotional trauma that is endured by children with sickle cell anemia.
Causes of death include bacterial infection (the most common cause), stroke or bleeding into the brain, and kidney, heart, or liver failure. The risk of bacterial infections does diminish after three years of age. Nevertheless, bacterial infections are the most common cause of death at any age. Therefore, any signs of infection in a person with sickle cell anemia must be reviewed with a doctor to prevent damage and save lives.
Interestingly, the sickle cell gene somewhat protects against malaria infection. This makes those with sickle cell trait (gene carriers) at least partially resistant to malaria. Furthermore, the geographic distribution of the sickle cell gene is similar to that of malaria infection. Sickle cell anemia is a lethal condition that threatens life. But there may be a selective advantage to being a sickle cell carrier (trait) if the person resides in an area of the world where malaria is very common. The advantage a person with sickle cell trait has over a non-carrier of the gene may explain why sickle cell anemia did not disappear from the world even though it is lethal.
The sickle cell gene is not a "black gene." It just happens to disproportionately occur in the black population. When a black person who carries a sickle cell gene has children with a non-black person, the children may inherit the sickle cell gene regardless of their color. There are also non-black persons who carry the sickle cell gene.
Recent research is examining further ways to promote the development of the fetal hemoglobin that delays the development of sickle cell in the newborn. Bone marrow transplantation is being used for patients with severe sickle cell anemia who have a genetically identical sibling that can offer the transplant marrow. Future treatments may involve genetic engineering where cures might be achieved.
Finally, genetic counseling can be helpful for parents and families to prevent sickle cell anemia. Sickle cell anemia is an inherited illness. Both parents must be carriers of the sickle cell gene for a child to be affected with sickle cell anemia. If each parent is a carrier, any child has a one chance in two (50%) of also being a carrier and a one in four (25%) chance of inheriting both genes from the parents and being affected with sickle cell anemia.

Sickle Cell Anemia At A Glance

Sickle cell anemia is an inherited disorder of the hemoglobin in blood.
Sickle cell anemia requires the inheritance of two sickle cell genes.
Sickle cell trait, which is the inheritance of one sickle gene, almost never causes problems.
Virtually all of the major symptoms of sickle cell anemia are the direct result of the abnormally shaped sickled red blood cells blocking the flow of blood.
The current treatment of sickle cell anemia is directed primarily toward managing the individual features of the illness as they occur.

Reference:
Bunn, HF. Pathogenesis and treatment of sickle cell disease. N Engl J Med 1997; 337:762.
Harrison's Principles of Internal Medicine, McGraw-Hill, edited by Eugene Braunwald, et. al., 2001.
Source:Medicinenet.com.

Medical Author:

William C. Shiel Jr., MD, FACP, FACR

Peripheral Vascular Disease (PVD, Peripheral Artery Disease, Peripheral Arterial Disease, PAD)

2012-03-17T03:55:00.001-07:00

What is peripheral vascular disease?

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.

What is 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.

How does atherosclerosis cause disease?

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.

What are complications of peripheral artery disease?

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.

What are the other causes of peripheral vascular diseases?

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.

Who is at risk for 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:

High blood levels of the bad LDL cholesterol and triglycerides
Low blood levels of the good HDL cholesterol
Cigarette smoking
Diabetes mellitus (both Type I and Type II diabetes)
High blood pressure (hypertension) or a family history of hypertension
A family history of atherosclerotic disease
Chronic renal failure
Overweight or obesity
Physical inactivity

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.

What are the symptoms and signs of peripheral artery disease?

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.

Intermittent claudication - Intermittent claudication refers to pain or cramping in the arms or legs that occurs with exercise and subsides with rest. The severity and location of the pain of intermittent claudication vary depending upon the location and extent of blockage of the involved artery. The most common location of intermittent claudication is the calf muscle. The pain in the calf muscle occurs only during exercise such as walking, and the pain steadily increases with continued walking until the patient has to stop due to intolerable pain. Then the pain quickly subsides during rest. Intermittent claudication can affect one or both legs.

Rest pain - Rest pain occurs when the artery occlusion is so critical that there is not enough blood and oxygen supply to the lower extremities even at rest. The pain typically affects the feet, is usually severe, and occurs at night when the patient assumes a supine position (lying down, face up).

Other symptoms and signs of peripheral artery disease include:

Numbness of the extremities
Weakness and atrophy (diminished size and strength) of the calf muscle
A feeling of coldness in the legs or feet
Changes in color of the feet; feet turn pale when they are elevated, and turn dusky red in dependent position
Hair loss over the dorsum of the feet and thickening of the toenails
Painful ulcers and/or gangrene in tissue where there is critical ischemia; typically in the toes.

How is peripheral artery disease diagnosed?

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:

Doppler ultrasound - A form of ultrasound (measurement of high-frequency sound waves that are reflected off of tissues) that can detect and measure blood flow. Doppler ultrasound is used to measure blood pressures behind the knees and at the ankles. In patients with significant peripheral artery disease in the legs, the blood pressures in the ankles will be lower than the blood pressure in the arms (brachial blood pressure). The ankle-brachial index (ABI) is a number derived from dividing the ankle blood pressure by the brachial blood pressure. ABI of .9 to 1.3 is normal, ABI less than 0.9 indicate the presence of peripheral artery disease in the arteries in the legs, and ABI below 0.5 usually indicates severe arterial occlusion in the legs.
Duplex ultrasound - is a color assisted non-invasive technique to study the arteries. Ultrasound probes can be placed on the skin overlying the arteries and can accurately detect the site of artery stenosis as well as measure the degree of obstruction.
Angiography - An angiography is an imaging procedure to study the blood vessels similar to coronary angiogram. It is the most accurate test to detect the location(s) and severity of artery occlusion, as well as collateral circulations. Small hollow plastic tubes (catheters) are advanced from a small skin puncture at the groin (or the arm), under x-ray guidance, to the aorta and the arteries. Iodine contrast "dye," is then injected into the arteries while an x-ray video is recorded. Angiogram gives the doctor a picture of the location and severity of narrowed artery segments. This information is important in helping the doctor select patients for angioplasty or surgical bypass (see below).

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.

Magnetic resonance imaging (MRI) angiography uses magnetism, radio waves, and a computer to produce images of body structures and has the advantage of avoiding x-ray radiation exposure.

What are the treatments for peripheral artery disease?

Treatment goals for peripheral artery disease include:

Relieve the pain of intermittent claudication.
Improve exercise tolerance by increasing the walking distance before the onset of claudication.
Prevent critical artery occlusion that can lead to foot ulcers, gangrene, and amputation.
Prevent heart attacks and strokes.

Treatments of peripheral artery disease include lifestyle measures, supervised exercises, medications, angioplasty, and surgery.

Lifestyle changes

Smoking cessation eliminates a major risk factor for disease progression and lowers the incidences of rest pain and need for amputations. Smoking cessation is also important for the prevention of heart attacks and strokes.
A healthy diet can help lower blood cholesterol and other lipid levels and may help control blood pressure.
Diabetes control
Blood pressure control
Lipid control

Supervised exercise

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.

Medications

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.

Antiplatelet medications [such as aspirin and clopidogrel (Plavix)] make the blood platelets less likely to stick to one another to form blood clots. Low dose aspirin (81-325 mg/day) is usually prescribed indefinitely because it is also helpful in preventing strokes and heart attacks in patients with peripheral artery disease. Clopidogrel (Plavix) is an alternative to aspirin for those who are allergic or cannot tolerate aspirin. Anti-platelet medications also help prevent occlusion of blood vessels after angioplasty or bypass surgery.

Anticoagulant medications act to prevent blood clotting. Both heparin and warfarin (Coumadin) are anticoagulant medications. Anticoagulants are sometimes prescribed for people with peripheral artery disease if they are at increased risk for formation of blood clots; these agents are used much less frequently than anti platelet agents in patients with PAD.

Cholesterol-lowering drugs of the statin family have been shown in numerous large clinical trials to help prevent heart attacks and strokes and prolong survival among patients with atherosclerosis. Statins have also been shown to slow the progression of peripheral artery disease, decrease arthrosclerosis in the arteries, and improve claudication symptoms. Current NCEP recommendations for patients with peripheral artery disease are to use diet and medications (such as statins) to lower LDL cholesterol to below 100 mg/dl. Many doctors are now recommending lowering LDL cholesterol even further for patients with peripheral artery disease to below 75-80 mg/dl.

Cilostazol (Pletal) is a mediation that can help increase physical activity (enabling one to walk a greater distance without the pain of claudication). Cilostazol works by causing dilation of the arteries and an increased supply of oxygenated blood to be delivered to the arms and legs. Cilostazol is recommended for some patients with claudication when lifestyle modifications and exercise are ineffective. Cilostazol should be taken on an empty stomach either a half an hour before or two hours after meals. High fat meals, grapefruit juice, and certain medications such as omeprazole (Prilosec) and diltiazem (Cardizem) can increase the absorption and hence the blood levels of Cilostazol. Side effects are generally mild that include headache, diarrhea and dizziness. Cilostazol should not be used in patients with heart failure because of concern over increased mortality in heart failure patients using medications similar to Cilostazol.

Pentoxifylline (Pentoxyl, Trental) was designed and approved to improve blood flow to the extremities by decreasing the viscosity ("stickiness") of blood, enabling more efficient blood flow. Pentoxifylline, in clinical trials, improved walking distance, but its benefits are weaker than those of Cilostazol and have not been conclusively proved by all studies.

Drugs to control hypertension may also be prescribed. There was concern that beta blockers used to treat hypertension can aggravate claudication. But recent studies have not found any adverse effects of beta-blockers on symptoms of patients with peripheral artery disease. Therefore current recommendations are to treat hypertension in patients with peripheral artery disease to prevent strokes and heart attacks.

Angioplasty

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.

Surgery

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.

Peripheral Vascular Disease At A Glance

The term peripheral vascular disease is commonly used to refer to peripheral artery disease (PAD), meaning narrowing or occlusion by atherosclerotic plaques of arteries outside of the heart and brain.
Risk factors for peripheral artery disease include elevated blood cholesterol, diabetes, smoking, hypertension, inactivity, and overweight/obesity.
About 5% of people over the age of 50 are believed to suffer from peripheral artery disease.
The symptoms of peripheral artery disease depend upon the location and extent of the blocked arteries. The most common symptom of peripheral artery disease is intermittent claudication, manifested by pain (usually in the calf) that occurs while walking and dissipates at rest.
Doctors may use radiologic imaging techniques including Doppler ultrasound, and angiography to aid in the diagnosis of peripheral artery disease.
Peripheral artery disease can be treated by lifestyle alterations, medications, angioplasty and related treatments, or surgery.
Complications of peripheral artery disease include sores that do not heal, ulcers, gangrene, or infections in the extremities. In rare cases, amputation may be necessary.
Having peripheral artery disease usually indicates the potential for arterial disease involving the coronary arteries within the brain.

Medical Author:

Melissa Conrad Stöppler, MD

Medical Editor:

Dennis Lee, MD

Medical Editor:

Daniel Lee Kulick, MD, FACC, FSCAI
Source:Medicinenet.com.

Heart Attack Pathology (Photo Essay)

2012-03-17T03:50:00.001-07:00

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.
Can a person have more than one Heart Attack?
Yes. Not uncommonly, people with coronary artery disease have more than one heart attack over the years. In fact, by looking at the heart tissue at autopsy, pathologists can tell when myocardial infarctions occurred. Thus, very recent (acute, hours old) infarctions may appear as a pale brown region, infarctions days old (subacute) appear yellow, and healed (weeks to years old) infarctions appear as white scars in the heart muscle. Figure 5 shows three myocardial infarctions of different ages in the muscle of a left ventricle.
Figure 5: Three Myocardial Infarctions of Different Ages
Slice Across Heart Ventricles

Source:Medicinenet.com.

Medical Author:

Michael C. Fishbein, MD

Medical Editor:

Leslie J. Schoenfield, MD, PhD

Medical Reviewer:

Jay W. Marks, MD

Vitamins & Exercise Heart Attack Prevention Series

2012-03-17T03:48:00.001-07:00

Folic acid, B vitamins, and homocysteine

Homocysteine is metabolized (chemically transformed) into methionine and cysteine with the help of the B vitamins; folic acid, B12, and B6 (pyridoxine). Therefore, insufficient amounts of these B vitamins in the body can theoretically hamper the metabolic breakdown of homocysteine, and hence increase its blood levels. High levels of homocysteine in the blood (hyperhomocysteinemia) can damage the inner surface of blood vessels, promote blood clotting, and accelerate atherosclerosis.
The current state of knowledge regarding folic acid, homocysteine, and heart attacks is as follows:

The level of blood folate is an important determinant of the blood homocysteine level. Low blood folate levels are associated with high blood levels of homocysteine.
Low blood folate is common among individuals who do not take multivitamins, but unusual among those who do.
The consumption of folic acid supplements or folic acid fortified cereals can increase blood folate levels and decrease blood homocysteine levels.
In a large population study involving women, those who had the highest consumption of folic acid (usually in the form of multivitamins) had fewer heart attacks than those who consumed the least amount of folic acid.

Even though current scientific evidence suggests that taking folic acid and vitamin B supplements to lower homocysteine levels should help prevent atherosclerosis and heart attacks, conclusive proof is still lacking because:

There are no conclusive controlled studies (discussed at the beginning of this article) demonstrating that increasing folic acid intake actually prevents atherosclerosis and heart attacks.
There is no clinical study demonstrating that lowering blood levels of homocysteine actually prevents atherosclerosis and heart attacks.

There is also no official recommendation as to who should be tested for hyperhomocysteinemia. The optimal doses of the B vitamins, folic acid, B12, and B6, required to prevent and treat hyperhomocysteinemia are also uncertain. For folic acid, a daily dose of 0.8-1.0 mg is probably adequate.

What about antioxidants for heart attack prevention?

Antioxidants are food supplements that have been promoted as preventing heart disease and stroke. An important early event in the development of a cholesterol plaque in atherosclerosis is the oxidative modification of LDL cholesterol (low density lipoprotein) particles in the blood and the subsequent interaction of this modified LDL with the wall of the coronary artery. This process initiates the formation of the cholesterol plaque.
Antioxidants that block the oxidative modification of LDL have been shown to slow the progression of atherosclerosis in animal experiments. Examples of antioxidants include vitamin E and beta carotene. In humans, observational studies (studies that observe the frequency of related conditions) have found a relationship between the dietary intake of vitamin E and lower rates of heart attacks.
Observational studies provide only circumstantial evidence, however, and credible evidence is obtained only by way of controlled trials (discussed at the beginning of this article). Several controlled trials performed to date have yielded conflicting results on the benefits of antioxidant therapy. These results may possibly be due to the low doses of vitamin E used, the small number of patients in the study, or the limited duration of treatment.
The Heart Outcomes Prevention Evaluation study used a high dose (400 IU per day) of vitamin E over a span of five years in patients with significant risk factors for heart disease or stroke. This study found no difference in the occurrence of heart attack or stroke in the group treated with vitamin E versus those given the placebo. This study demonstrated that antioxidant therapy does not have any benefit in persons who have or are at high risk for having atherosclerosis.

How about exercise for heart attack prevention?

Studies of the effects of exercise in preventing heart attacks have yielded conflicting results. This is likely due to the fact that people who exercise regularly generally have healthier lifestyles and that many risk factors for heart disease can be influenced by exercise. Therefore, the specific role of exercise itself in heart attack prevention is difficult to isolate. For example, regular exercise has direct effects on weight control, blood pressure, diabetes, blood cholesterol, and smoking.

What about smoking cessation for heart attack prevention?

Smoking cessation, by whatever means, has been clearly demonstrated to reduce future heart attacks and death in patients with known coronary artery disease or who have other risk factors for the development of coronary artery disease. While many methods, both chemical and behavioral, have been used to aid smoking cessation, the initial success rate is often low, and the relapse rate is high. Certain medications that affect neurotransmitters in the brain, which are similar to agents often used to treat depression [for example, bupropion (Wellbutrin, Wellbutrin SR, Wellbutrin XL, Zyban)], have recently been demonstrated to be helpful in many patients trying to stop smoking. While effective, these agents may produce significant side effects and should only be used under the close supervision of a doctor.

Recommendations to prevent heart attacks

Eat whole, natural, and fresh foods.
Eat five to ten servings of fruits and vegetables daily and eat more peas, beans, and nuts.
Increase intake of omega-3 fatty acids by eating more fish, walnuts, flaxseed oil, and green leafy vegetables. An example of meeting the recommended intake of omega-3 fats is to eat 2 salmon portions a week or 1 gram of omega-3-fatty acid supplement daily.
Drink water, tea, non-fat dairy and red wine (two drinks or less daily for men, one drink or less daily for women).
Eat lean protein such as skinless poultry, fish, and lean cuts of red meat.
Avoid trans-fats and limit intake of saturated fats. This means avoiding fried foods, hard margarine, commercial baked goods, and most packaged and processed snack foods, high fat dairy and processed meats such as bacon, sausage, and deli meats.
Limit glycemic foods. Glycemic foods are those made with sugar and white flour, which increase blood sugar levels. Increased blood sugar levels stimulate the pancreas to release insulin. Chronically high insulin levels are believed to cause weight gain as well as atherosclerosis of the arteries.
Exercise daily.

Reference:
The HOPE and HOPE-TOO Trial Investigators. Effects of Long-term vitamin E supplementation on cardiovascular events and cancer: A randomized controlled trial. JAMA 293:1138-1347, 2005.

Source:Medicinenet.com.

Medical Author:

Daniel Lee Kulick, MD, FACC, FSCAI

Medical Author:

Dennis Lee, MD

Medical Editor:

William C. Shiel Jr., MD, FACP, FACR

Congestive Heart Failure

2012-03-17T03:47:00.001-07:00

Congestive heart failure facts

Congestive heart failure (CHF) is a condition in which the heart's function as a pump is inadequate to meet the body's needs.

Many disease processes can impair the pumping efficiency of the heart to cause congestive heart failure.

The symptoms of congestive heart failure vary, but can include fatigue, diminished exercise capacity, shortness of breath, and swelling.

The diagnosis of congestive heart failure is based on knowledge of the individual's medical history, a careful physical examination, and selected laboratory tests.

The treatment of congestive heart failure can include lifestyle modifications, addressing potentially reversible factors, medications, heart transplant, and mechanical therapies.

The course of congestive heart failure in any given patient is extremely variable.

What is congestive heart failure?

Congestive heart failure (CHF) is a condition in which the heart's function as a pump is inadequate to deliver oxygen rich blood to the body. Congestive heart failure can be caused by:

diseases that weaken the heart muscle,
diseases that cause stiffening of the heart muscles, or
diseases that increase oxygen demand by the body tissue beyond the capability of the heart to deliver adequate oxygen-rich blood.

The heart has two atria (right atrium and left atrium) that make up the upper chambers of the heart, and two ventricles (left ventricle and right ventricle) that make up the lower chambers of the heart. The ventricles are muscular chambers that pump blood when the muscles contract. The contraction of the ventricle muscles is called systole.
Many diseases can impair the pumping action of the ventricles. For example, the muscles of the ventricles can be weakened by heart attacks, infections (myocarditis) or toxins (alcohol, some chemotherapy agents). The diminished pumping ability of the ventricles due to muscle weakening is called systolic dysfunction. After each ventricular contraction (systole) the ventricle muscles need to relax to allow blood from the atria to fill the ventricles. This relaxation of the ventricles is called diastole.
Diseases such as hemochromatosis (iron overload) or amyloidosis can cause stiffening of the heart muscle and impair the ventricles' capacity to relax and fill; this is referred to as diastolic dysfunction. The most common cause of this is longstanding high blood pressure resulting in a thickened (hypertrophied) heart. Additionally, in some patients, although the pumping action and filling capacity of the heart may be normal, abnormally high oxygen demand by the body's tissues (for example, with hyperthyroidism or anemia) may make it difficult for the heart to supply an adequate blood flow (called high output heart failure).
In some individuals one or more of these factors can be present to cause congestive heart failure. The remainder of this article will focus primarily on congestive heart failure that is due to heart muscle weakness, systolic dysfunction.
Congestive heart failure can affect many organs of the body. For example:

The weakened heart muscles may not be able to supply enough blood to the kidneys, which then begin to lose their normal ability to excrete salt (sodium) and water. This diminished kidney function can cause the body to retain more fluid.
The lungs may become congested with fluid (pulmonary edema) and the person's ability to exercise is decreased.
Fluid may likewise accumulate in the liver, thereby impairing its ability to rid the body of toxins and produce essential proteins.
The intestines may become less efficient in absorbing nutrients and medicines.
Fluid also may accumulate in the extremities, resulting in edema (swelling) of the ankles and feet.

Eventually, untreated, worsening congestive heart failure will affect virtually every organ in the body.
Picture of the heart and valves, left and right ventricles, left and right atria

What causes congestive heart failure?

Many disease processes can impair the pumping efficiency of the heart to cause congestive heart failure. In the United States, the most common causes of congestive heart failure are:

coronary artery disease
high blood pressure (hypertension)
longstanding alcohol abuse
disorders of the heart valves
unknown (idiopathic) causes, such as after recovery from myocarditis

Less common causes include viral infections of the stiffening of the heart muscle, thyroid disorders, disorders of the heart rhythm, and many others.
It should also be noted that in patients with underlying heart disease, taking certain medications can lead to the development or worsening of congestive heart failure. This is especially true for those drugs that can cause sodium retention or affect the power of the heart muscle. Examples of such medications are the commonly used nonsteroidal anti-inflammatory drugs (NSAIDs), which include ibuprofen (Motrin and others) and naproxen (Aleve and others) as well as certain steroids, some medication for diabetes (such as rosiglitazone [Avandia] or pioglitazone [Actos]), and some calcium channel blockers.

What are the symptoms of congestive heart failure?

The symptoms of congestive heart failure vary among individuals according to the particular organ systems involved and depending on the degree to which the rest of the body has "compensated" for the heart muscle weakness.

An early symptom of congestive heart failure is fatigue. While fatigue is a sensitive indicator of possible underlying congestive heart failure, it is obviously a nonspecific symptom that may be caused by many other conditions. The person's ability to exercise may also diminish. Patients may not even sense this decrease and they may subconsciously reduce their activities to accommodate this limitation.
As the body becomes overloaded with fluid from congestive heart failure, swelling (edema) of the ankles and legs or abdomen may be noticed. This can be referred to as "right sided heart failure" as failure of the right sided heart chambers to pump venous blood to the lungs to acquire oxygen results in buildup of this fluid in gravity-dependent areas such as in the legs. The most common cause of this is longstanding failure of the left heart, which may lead to secondary failure of the right heart. Right-sided heart failure can also be caused by severe lung disease (referred to as "cor pulmonale"), or by intrinsic disease of the right heart muscle (less common)
In addition, fluid may accumulate in the lungs, thereby causing shortness of breath, particularly during exercise and when lying flat. In some instances, patients are awakened at night, gasping for air.
Some may be unable to sleep unless sitting upright.
The extra fluid in the body may cause increased urination, particularly at night.
Accumulation of fluid in the liver and intestines may cause nausea, abdominal pain, and decreased appetite.

How is congestive heart failure diagnosed?

The diagnosis of congestive heart failure is most often a clinical one that is based on knowledge of the patient's pertinent medical history, a careful physical examination, and selected laboratory tests.
A thorough patient history may disclose the presence of one or more of the symptoms of congestive heart failure described above. In addition, a history of significant coronary artery disease, prior heart attack, hypertension, diabetes, or significant alcohol use can be clues.
The physical examination is focused on detecting the presence of extra fluid in the body (breath sounds, leg swelling, or neck veins) as well as carefully characterizing the condition of the heart (pulse, heart size, heart sounds, and murmurs).
Useful diagnostic tests include the electrocardiogram (ECG) and chest X-ray to detect previous heart attacks, arrhythmia, heart enlargement, and fluid in and around the lungs. Perhaps the single most useful diagnostic test is the echocardiogram, in which ultrasound is used to image the heart muscle, valve structures, and blood flow patterns. The echocardiogram is very helpful in diagnosing heart muscle weakness. In addition, the test can suggest possible causes for the heart muscle weakness (for example, prior heart attack, and severe valve abnormalities). Virtually all patients in whom the diagnosis of congestive heart failure is suspected should ideally undergo echocardiography early in their assessment.
Nuclear medicine studies assess the overall pumping capability of the heart and examine the possibility of inadequate blood flow to the heart muscle. Heart catheterization allows the arteries to the heart to be visualized with angiography (using dye inside of the blood vessels that can be seen using X-ray methods). During catheterization the pressures in and around the heart can be measured and the heart's performance assessed. In rare cases, a biopsy of the heart tissue may be recommended to diagnose specific diseases. This biopsy can often be accomplished through the use of a special catheter device that is inserted into a vein and maneuvered into the right side of the heart.
Another helpful diagnostic test is a blood test called a BNP or B-type natriuretic peptid level. This level can vary with age and gender but is typically elevated from heart failure and can aid in the diagnosis, and can be useful in following the response to treatment of congestive heart failure.
The choice of tests depends on each patient's case and is based on the suspected diagnoses.

What is the treatment of congestive heart failure?

Lifestyle modifications

After congestive heart failure is diagnosed, treatment should be started immediately. Perhaps the most important and yet most neglected aspect of treatment involves lifestyle modifications. Sodium causes an increase in fluid accumulation in the body's tissues. Because the body is often congested with excess fluid, patients become very sensitive to the levels of intake of sodium and water. Restricting salt and fluid intake is often recommended because of the tendency of fluid to accumulate in the lungs and surrounding tissues. An American "no added salt" diet can still contain 4 to 6 grams (4000 to 6000 milligrams) of sodium per day. In individuals with congestive heart failure, an intake of no more than 2 grams (2000 milligrams) of sodium per day is generally advised. Reading food labels and paying close attention to total sodium intake is very important. Severe restriction of alcohol consumption also is advised.
Likewise, the total amount of fluid consumed must be regulated. Although many people with congestive heart failure take diuretics to aid in the elimination of excess fluid, the action of these medications can be overwhelmed by an excess intake of water and other fluids. The maxim that "drinking eight glasses of water a day is healthy" certainly does not apply to patients with congestive heart failure. In fact, patients with more advanced cases of congestive heart failure are often advised to limit their total daily fluid intake from all sources to 2 quarts. The above guidelines for sodium and fluid intake may vary depending on the severity of congestive heart failure in any given individual and should be discussed with their physician.
An important tool for monitoring an appropriate fluid balance is the frequent measurement of body weight. An early sign of fluid accumulation is an increase in body weight. This may occur even before shortness of breath or swelling in the legs and other body tissues (edema) is detected. A weight gain of two to three pounds over two to three days should prompt a call to the physician, who may order an increase in the dose of diuretics or other methods designed to stop the early stages of fluid accumulation before it becomes more severe.
Aerobic exercise, once discouraged for congestive heart failure patients, has been shown to be beneficial in maintaining overall functional capacity, quality of life, and perhaps even improving survival. Each person's body has its own unique ability to compensate for the failing heart. Given the same degree of heart muscle weakness, individuals may display widely varying degrees of limitation of function. Regular exercise, when tailored to the person's tolerance level, appears to provide significant benefits and should be used only when the individual is compensated and stable.
Addressing potentially reversible factors
Depending on the underlying cause of congestive heart failure, potentially reversible factors should be explored. For example:

In certain persons whose congestive heart failure is caused by inadequate blood flow to the heart muscle, restoration of the blood flow through coronary artery surgery or catheter procedures (angioplasty, intracoronary stenting) may be considered.
Congestive heart failure that is due to severe disease of the valves may be alleviated by valve surgery in appropriate patients.
When congestive heart failure is caused by chronic, uncontrolled high blood pressure (hypertension), aggressive blood pressure control will often improve the condition.
Heart muscle weakness that is due to longstanding, severe alcohol abuse can improve significantly with abstinence from drinking.
Congestive heart failure that is caused by other disease states may be similarly partially or completely reversible by appropriate measures.

Medications

Until recently, the selection of medications available for the treatment of congestive heart failure was frustratingly limited and focused mainly on controlling the symptoms. Medications have now been developed that both improve symptoms, and, importantly, prolong survival.
Angiotensin Converting Enzyme (ACE) Inhibitors

ACE inhibitors have been used for the treatment of hypertension for more than 20 years. This class of drugs has also been extensively studied in the treatment of congestive heart failure. These medications block the formation of angiotensin II, a hormone with many potentially adverse effects on the heart and circulation in patients with heart failure. In multiple studies of thousands of patients, these drugs have demonstrated a remarkable improvement of symptoms in patients, prevention of clinical deterioration, and prolongation of survival. In addition, they have been recently been shown to prevent the development of heart failure and heart attacks. The wealth of the evidence supporting the use of these agents in heart failure is so strong that ACE inhibitors should be considered in all patients with heart failure, especially those with heart muscle weakness.
Possible side effects of these drugs include:

a nagging, dry cough,
low blood pressure,
worsening kidney function and electrolyte imbalances, and
rarely, true allergic reactions.

When used carefully with proper monitoring, however, the majority of individuals with congestive heart failure tolerate these medications without significant problems. Examples of ACE inhibitors include:

captopril (Capoten),
enalapril (Vasotec),
lisinopril (Zestril, Prinivil),
benazepril (Lotensin), and
ramipril (Altace).

For those individuals who are unable to tolerate the ACE inhibitors, an alternative group of drugs, called the angiotensin receptor blockers (ARBs), may be used. These drugs act on the same hormonal pathway as the ACE inhibitors, but instead block the action of angiotensin II at its receptor site directly. A small, early study of one of these agents suggested a greater survival benefit in elderly congestive heart failure patients as compared to an ACE inhibitor. However, a larger, follow-up study failed to demonstrate the superiority of the ARBs over the ACE inhibitors. Further studies are underway to explore the use of these agents in congestive heart failure both alone and in combination with the ACE inhibitors.
Possible side effects of these drugs are similar to those associated with the ACE inhibitors, although the dry cough is much less common. Examples of this class of medications include:

losartan (Cozaar),
candesartan (Atacand),
telmisartan (Micardis),
valsartan (Diovan),
irbesartan (Avapro), and
olmesartan (Benicar).

Beta-blockers
Certain hormones, such as epinephrine (adrenaline), norepinephrine, and other similar hormones, act on the beta receptor's of various body tissues and produce a stimulative effect. The effect of these hormones on the beta receptors of the heart is a more forceful contraction of the heart muscle. Beta-blockers are agents that block the action of these stimulating hormones on the beta receptors of the body's tissues. Since it was assumed that blocking the beta receptors further depressed the function of the heart, beta-blockers have traditionally not been used in persons with congestive heart failure. In congestive heart failure, however, the stimulating effect of these hormones, while initially useful in maintaining heart function, appears to have detrimental effects on the heart muscle over time.
However, studies have demonstrated an impressive clinical benefit of beta-blockers in improving heart function and survival in individuals with congestive heart failure who are already taking ACE inhibitors. It appears that the key to success in using beta-blockers in congestive heart failure is to start with a low dose and increase the dose very slowly. At first, patients may even feel a little worse and other medications may need to be adjusted.
Possible side effects include:

fluid retention,
low blood pressure,
low pulse, and
general fatigue and lightheadedness.

Beta-blockers should generally not be used in people with certain significant diseases of the airways (for example, asthma, emphysema) or very low resting heart rates. While carvedilol (Coreg) has been the most thoroughly studied drug in the setting of congestive heart failure, studies of other beta-blockers have also been promising. Research comparing carvedilol directly with other beta-blockers in the treatment of congestive heart failure is ongoing. Long acting metoprolol (Toprol XL) is also very effective in individuals with congestive heart failure.
Digoxin
Digoxin (Lanoxin) has been used in the treatment of congestive heart failure for hundreds of years. It is naturally produced by the foxglove flowering plant. Digoxin stimulates the heart muscle to contract more forcefully. It also has other actions, which are not completely understood, that improve congestive heart failure symptoms and can prevent further heart failure. However, a large-scale randomized study failed to demonstrate any effect of digoxin on mortality.
Digoxin is useful for many patients with significant congestive heart failure symptoms, even though long-term survival may not be affected. Potential side effects include:

nausea,
vomiting,
heart rhythm disturbances,
kidney dysfunction, and
electrolyte abnormalities.

These side effects, however, are generally a result of toxic levels in the blood and can be monitored by blood tests. The dose of digoxin may also need to be adjusted in patients with significant kidney impairment.
Diuretics
Diuretics are often an important component of the treatment of congestive heart failure to prevent or alleviate the symptoms of fluid retention. These drugs help keep fluid from building up in the lungs and other tissues by promoting the flow of fluid through the kidneys. Although they are effective in relieving symptoms such as shortness of breath and leg swelling, they have not been demonstrated to positively impact long-term survival.
Nevertheless, diuretics remain key in preventing deterioration of the patient's condition thereby requiring hospitalization. When hospitalization is required, diuretics are often administered intravenously because the ability to absorb oral diuretics may be impaired, when congestive heart failure is severe. Potential side effects of diuretics include:

dehydration,
electrolyte abnormalities,
particularly low potassium levels,
hearing disturbances, and
low blood pressure.

It is important to prevent low potassium levels by taking supplements, when appropriate. Such electrolyte disturbances may make patients susceptible to serious heart rhythm disturbances. Examples of various classes of diuretics include:

furosemide (Lasix),
hydrochlorothiazide (Hydrodiuril),
bumetanide (Bumex),
torsemide (Demadex),
spironolactone (Aldactone), and
metolazone (Zaroxolyn).

One particular diuretic has been demonstrated to have surprisingly favorable effects on survival in congestive heart failure patients with relatively advanced symptoms. Spironolactone (Aldactone) has been used for many years as a relatively weak diuretic in the treatment of various diseases. Among other things, this drug blocks the action of the hormone aldosterone.
Aldosterone has many theoretical detrimental effects on the heart and circulation in congestive heart failure. Its release is stimulated in part by angiotensin II (see ACE inhibitors, above). In patients taking ACE inhibitors, however, there is an "escape" phenomenon in which aldosterone levels can increase despite low levels of angiotensin II. Medical researchers have found that spironolactone (Aldactone) can improve the survival rate of patients with congestive heart failure. In that the doses used in the study were relatively small, it has been theorized that the benefit of the drug was in its ability to block the effects of aldosterone rather than its relatively weak action as a diuretic (water pill). Possible side effects of this drug include elevated potassium levels and, in males, breast tissue growth (gynecomastia).
Another aldosterone inhibitor is eplerenone (Inspra).

Heart transplant

In some cases, despite the use of optimal therapies as described above, the patient's condition continues to deteriorate due to progressive heart failure. In selected patients, heart transplantation is a viable treatment option. Candidates for heart transplantation are generally under age 70 and do not have severe or irreversible diseases affecting the other organs. Additionally, a transplant is done only when it is clear that the patient's prognosis is poor with continued medical treatment of the heart condition. Transplant patients require close medical follow-up while taking the necessary drugs that suppress the immune system, and because of the risk of rejection of the transplanted heart. They also must be monitored for possible development of coronary artery disease in the transplanted heart.
Although there are thousands of patients on waiting lists for a heart transplant at any given time, the number of operations performed each year is limited by the number of available donor organs. For these reasons, heart transplantation is a realistic option in only a small subset of the large numbers of patients with congestive heart failure.

Other mechanical therapies

Given the limitations associated with heart transplantation, much attention has recently been directed towards the development of mechanical assist devices that are designed to assume part or all of the pumping function of the heart. There are several devices available for clinical use and many more are actively being developed. For instance, there are currently left ventricular assist devices that are approved for use as a temporary mode of circulatory support in very ill patients until a transplant can be performed. Studies examining the possible role of these mechanical assist devices on a long term basis as permanent self-contained implants are ongoing. They may often be used for longer periods of time in older patients who may not be heart transplant candidates. The current major limitation of these devices is the risk of infection, especially at the site where the device exits the body through the skin to communicate with its external power source.
A less invasive modality, which can be placed without surgery, is the biventricular pacemaker. This device has proved valuable in appropriate types of patients with heart failure and impaired ventricles by improving the synchrony of contraction.

What is the long term prognosis for patients with congestive heart failure?

Congestive heart failure is generally a progressive disease with periods of stability punctuated by episodic clinical exacerbations. The course of the disease in any given individual, however, is extremely variable. Factors involved in determining the long term outlook (prognosis) for a given patient include:

the nature of the underlying heart disease,
the response to medications,
the degree to which other organ systems are involved and the severity of other accompanying conditions,
the person's symptoms and degree of impairment, and
other factors that remain poorly understood.

With the availability of newer drugs to potentially favorably affect the progression of disease, the prognosis in congestive heart failure is generally more favorable than that observed just 10 years ago. In some cases, especially when the heart muscle dysfunction has recently developed, a significant spontaneous improvement is not uncommonly observed, even to the point where heart function becomes normal.
Heart failure is often graded on a scale of I to IV based on the patient's ability to function.

Class I is patients with a weakened heart but without limitation or symptoms.
Class II is only limitation at heavier workloads.
Class III is limitation at everyday activity.
Class IV is severe symptoms at rest or with any degree of effort.

The prognosis of heart failure patients is very closely associated with the functional class.
An important issue in congestive heart failure is the risk of heart rhythm disturbances (arrhythmias). Of those deaths that occur in individuals with congestive heart failure, approximately 50% are related to progressive heart failure. Importantly, the other half are thought to be related to serious arrhythmias. A major advance has been the finding that nonsurgical placement of automatic implantable cardioverter/defibrillators (AICD) in individuals with severe congestive heart failure (defined by an ejection fraction below 30%-35%) can significantly improve survival, and has become the standard of care in most such individuals.
In some people with severe heart failure and certain ECG abnormalities, the left and right side of the heart don't beat in rhythm, and inserting a device called a biventricular pacer can significantly reduce symptoms.

What are the areas of new research in congestive heart failure?

Despite the significant advances in drug therapy for congestive heart failure over the past 20 years, many exciting developments are under active study. New classes of medications are being tested in clinical trials, including the calcium sensitizing agents, vasopeptidase inhibitors, and natriuretic peptides. As was the case with the ACE inhibitors and beta-blockers, the potential use of these drugs is based on theoretical considerations that have resulted from an increased understanding of the processes both underlying and resulting from heart failure. Additionally, gene therapy that is targeted toward certain genes thought to contribute to heart failure is being tested.
These developments have justified an unprecedented optimism in the treatment of congestive heart failure. The majority of individuals, with appropriate lifestyle measures and medical regimens, can maintain active, fulfilling lifestyles. The range of treatment options has been significantly strengthened by drugs such as the ACE inhibitors and beta-blockers. In the future, we will surely see the addition of many more and equally potent interventions.

REFERENCES:
Amsterdam EA. Revised American College of Cardiology/American Heart Association guidelines for the management of heart failure. Prev Cardiol. 2005 Fall;8(4):254, 256.

Heart Failure Society Of America. Evaluation and management of patients with acute decompensated heart failure. J Card Fail. 2006 Feb;12(1):e86-e103. Review.

Larson LW, Gerbert DA, Herman LM, Leger MM, McNellis R, O'Donoghue DL, Ulshafer C, Van Dyke EM; American College of Cardiology; American Heart Association. ACC/AHA 2005 guideline update: chronic heart failure in the adult. JAAPA. 2006 Apr;19(4):53-6.

Previous contributing editor: Dennis Lee, MD

Medical Author:

Daniel Lee Kulick, MD, FACC, FSCAI

Medical Editor:

William C. Shiel Jr., MD, FACP, FACR
Source:Medicinenet.com.

Heart Disease (Coronary Artery Disease)

2012-03-17T03:43:00.001-07:00

Heart disease facts

Coronary artery disease is the most common cause of death in the United States. Over a million people each year will have a heart attack and 25% will die before they get to the hospital while or in the Emergency Department.
Prevention is the key to treatment of heart disease.
Diagnosis of heart disease is often made by careful history taken by a health care practitioner. Some individuals may have atypical symptoms, including almost none at all.
The testing strategy to confirm the diagnosis and plan appropriate treatment needs to be individualized for each patient diagnosed with heart disease.
Treatment of heart disease depends upon the severity of disease, and is often directed by the symptoms experienced by the affected individual.

Introduction to heart disease

The heart is like any other muscle, requiring oxygen and nutrient-rich blood for it to function. The coronary arteries that supply blood to the heart muscle spread across the surface of the heart, beginning at the base of the aorta and branching out to all areas of the heart muscle.
The coronary arteries are at risk for narrowing as cholesterol deposits, called plaques, build up inside the artery. If the arteries narrow enough, blood supply to the heart muscle may be compromised (slowed down), and this slowing of blood flow to the heart causes pain, or angina.
A heart attack or myocardial infarction occurs when a plaque ruptures, allowing a blood clot to form. This completely obstructs the artery, stopping all blood flow to part of the heart muscle, and that portion of muscle dies.

What are the risk factors for heart disease?

Risk factors for heart disease include:

Smoking
High blood pressure (hypertension)
High cholesterol
Diabetes
Family history
Peripheral artery disease
Obesity

What are the symptoms of heart disease?

The typical symptoms of coronary artery disease are chest pain associated with shortness of breath. Classically, the pain of angina is described as a pressure or heaviness behind the breast bone with radiation to the jaw and down the arm accompanied by shortness of breath and sweating. Unfortunately, angina has a variety of signs and symptoms, and there may not even be specific chest pain. Other locations of pain and other symptoms may include shoulder or back ache, upper abdominal pain, nausea, and indigestion.
Women, the elderly, and people with diabetes may have different perceptions of pain or have no discomfort at all. Instead, they may complain of malaise or fatigue and generalized weakness and the inability to complete routine physical tasks such as walking or climbing stairs.
Health care practitioners and patients may have difficulty understanding each other when symptoms of angina are described. Patients may experience pressure or tightness but may deny any complaints of pain. Health care practitioners may misinterpret these symptoms when patient answers "no" to the question whether "pain is present," even though the patient is experiencing other types of discomfort.
People with coronary artery disease usually have gradual progression of their symptoms. As an artery narrows over time, the symptoms of decreased blood flow to part of the heart muscle may increase in frequency and/or severity. Health care practitioners may inquire about changes in exercise tolerance (How far can you walk before getting symptoms? Is it to the mailbox? Up a flight of stairs?), and whether there has been an acute change in the symptoms.
Once again, patients may be asymptomatic until a heart attack occurs. Of course, some patients also may be in denial as to their symptoms and procrastinate in seeking care.

How is heart disease diagnosed?

The diagnosis of heart disease begins with obtaining a history that the potential for coronary artery disease exists. Risk factors need to be assessed and risk stratification occurs. The type of testing that is recommended, if any, depends upon the potential that the patient's symptoms actually represent angina and are coming from the heart.
Heart disease tests
Not every patient with chest pain needs heart catheterization (the most invasive test). Instead, the healthcare provider will try to choose the testing modality that will best provide the diagnosis, and if coronary artery disease is present, decide what impairment, if any, is present.

Electrocardiogram (ECG or EKG)

The heart is an electrical pump, and the electrical impulses it generates can be detected on the surface of the skin. Normal muscle conducts electricity in a reproducible fashion. Muscle that has decreased blood supply conducts electricity poorly. Muscle that has lost its blood supply and has been replaced with scar tissue cannot conduct electricity. The electrocardiogram (EKG) is a noninvasive test used to reflect underlying heart conditions by measuring the electrical activity of the heart.
Some people have "abnormal" EKGs at baseline but this may be normal for them. It is important that an electrocardiogram be compared to previous tracings if one is available. If a patient has a baseline abnormal EKG, they should consider carrying a copy with them for reference should they ever need another EKG.

Stress testing

If the baseline EKG is relatively normal, then monitoring the EKG tracing while the patient exercises may uncover electrical changes that may indicate the presence of coronary artery disease. There are a variety of testing protocols used to determine whether the exercise intensity is high enough to prove that the heart is normal.
Some patients are unable to exercise on a treadmill, but they can still undergo cardiac stress testing by using intravenous medication that causes the heart to work harder.
Stress testing is done under the supervision of medical personnel because of the potential of provoking angina, shortness of breath, abnormal heart rhythms, and heart attack.

Echocardiography

Used with or without exercise, echocardiography can assess how the heart works. Using sound waves to generate an image, a cardiologist can evaluate many aspects of the heart. Echocardiograms can examine the structure of the heart including the heart valves, the thickness of the heart muscle, the septum (the tissues that separate the four heart chambers from each other) and the pericardial sac (the outside lining of the heart).
The test can indirectly assess blood flow to parts of the heart muscle. If there is decreased blood flow, then segments of the heart wall may not beat as strongly as adjacent heart muscle. These wall motion abnormalities signal the potential for coronary artery disease.
The echocardiogram can also assess the efficiency of the heart by measuring ejection fraction. Normally when the heart beats, it pushes more than 60% of the blood in the ventricle out to the body. Many diseases of the heart, including coronary artery disease, can decrease this percentage (the ejection fraction).

Perfusion studies

Radioactive chemicals like thallium or technetium can be injected into a vein and their uptake measured in heart muscle cells. Abnormally decreased uptake can signify decreased blood flow to parts of the heart because of coronary artery narrowing. This test may be used when the patient's baseline EKG is not normal and is less reliable when used to monitor a stress test.

Computerized tomography

The latest generation of CT scanners can take detailed images of blood vessels and may be used as an adjunct to determine whether coronary artery disease is present. In some institutions, the heart CT is used as a negative predictor. That means that the test is done to prove that the coronary arteries are normal rather than to prove that the disease is present.

Heart catheterization or coronary angiography

This test is the gold standard for the diagnosis of coronary artery disease. A cardiologist inserts and then threads a small tube through the groin or arm into the coronary arteries, where dye is injected to directly visualize the arteries on an x-ray. This test defines the anatomy of the coronary arteries. At the time of the catheterization, if blockages are found, they may be potentially treated with angioplasty in which a balloon is inflated to squash the plaque into the blood vessel wall and the insertion of a stent (wire cage that prevents the blood vessel from narrowing again).
CT coronary angiogram may be used test to diagnose coronary artery disease. During this procedure, intravenous dye containing iodine is injected into the patient and CT scanning is performed to image the coronary arteries.
Prior to the angiogram, a calcium score may be obtained. The calcium CT scan can measure the amount of calcium within heart blood vessels. If the score is 0, meaning that there is no calcium present, the risk of having heart disease is zero. The higher the score, the increased risk of narrowed coronary arteries.

What is the treatment for heart disease?

Coronary artery disease is usually treated in a multi-step approach depending upon a patient's symptoms. The patient and healthcare provider need to work together to return the patient to a normal lifestyle.

Prevention of heart disease

The key to the treatment is prevention. A healthy lifestyle includes exercise, proper nutrition, and smoking cessation. Moreover, controlling diabetes and high blood pressure to minimize contribution risk for heart disease is a major aspect of prevention.
An aspirin a day is recommended to decrease the risk for heart disease and should be started with the recommendation of a health care practitioner.
A little alcohol (one drink per day for women or two drinks per day for men) decreases the risk of heart disease compared to nondrinkers. However, it is not recommended that nondrinkers begin drinking.

Modifying risk factors for heart disease

While patients cannot choose their family and alter their genetic predisposition to coronary artery disease, the rest of the risk factors are under control of the patient. Keeping blood pressure, cholesterol and other lipid levels, and diabetes under control needs to become a life-long goal. Smoking cessation is highly encouraged.

Medications

The purpose of medications for coronary artery disease is to allow more efficient heart muscle function to overcome any blockage that might exist.
Aspirin is one of the cornerstones of coronary artery disease treatment. It prevents platelets from clumping together when blood becomes turbulent, like when it flows past a narrowing in an artery.
Beta blockers prevent the action of adrenaline on the heart and allow the heart to beat a more efficiently by reducing the heart rate and causing the heart muscle to contract less aggressively. Examples of beta blockers include:

atenolol (Tenormin)
metoprolol (Lopressor, Toprol XL)
propranolol (Inderal, Inderal LA)
carvedilol (Coreg)
labetalol (Normodyne, Trandate)

Calcium channel blockers can also be used to control heart rate and allow the heart to beat more efficiently. Examples of calcium channel blockers include:

diltiazem (Cardizem, Dilacor, Tiazac)
verapamil (Calan, Verelan, Verelan PM, Isoptin, Covera-HS)

Nitroglycerin dilates blood vessels and may be used sublingually, under the tongue, to treat angina. Some patients may be prescribed long-acting nitroglycerin to help control anginal symptoms.

Angioplasty and stenting

If the coronary angiogram (coronary=heart + angio=artery + gram=record) shows significant blockage in an artery, the cardiologist may attempt an angioplasty, in which a balloon is placed via a catheter (as with angiography) at the area of narrowing and when quickly inflated, compresses the offending plaque into the wall of the artery. Often a stent, or a metal cage, is placed at the site of angioplasty to keep the blood vessel from narrowing again. Should a stent be placed, patients are usually started on antiplatelet medication to prevent clot formation. Clopidogrel (Plavix) and prasugrel (Effient) are the two most common medications prescribed.

Surgery

For those patients with multiple coronary artery blockages, coronary artery bypass grafting may be a consideration.

REFERENCE: Ho JS, et al. Relation of a coronary artery calcium score higher than 400 to coronary stenoses detected using multidetector computed tomography and to traditional cardiovascular risk factors. Am J Cardiol. May 15 2008;101(10):1444-7.

Medical Author:

Benjamin Wedro, MD, FACEP, FAAEM

Medical Editor:

Daniel Lee Kulick, MD, FACC, FSCAI

Medical Editor:

Melissa Conrad Stöppler, MD

Source:Medicinenet.com.

Digestive Diseases: Bowel Incontinence

2012-03-16T01:57:00.000-07:00

Introduction to Bowel Incontinence

Bowel or fecal incontinence is the loss of voluntary control of stool, or bowel movements. This condition can vary from being partial, in which a person loses only a small amount of liquid waste, to complete, in which the entire solid bowel movement cannot be controlled.
Bowel incontinence affects more than 5.5 million Americans. Both men and women suffer from this problem, though it is more common in women because of injury to the anal muscles or nerves that can occur during childbirth. Bowel incontinence becomes more common with advancing age as the muscles that control bowel movements (anal sphincter muscles) weaken.
Often, embarrassment and the stigma associated with incontinence prevent people from seeking treatment, even when incontinence affects his or her quality of life. Many people resort to altering their social and physical activities, even their employment, to cope with the problem. In addition, some people with bowel incontinence do not see a doctor because they just don't realize that their problem can be effectively treated. It's important to understand that bowel incontinence is not uncommon and can be successfully treated.

What Causes Bowel Incontinence?

Normal control of bowel movements depends on proper functioning of the colon and rectum, the muscles surrounding the anus (anal sphincter muscles), the brain and the body's nerves (the nervous system), plus the amount and consistency of waste products produced.
There are many causes of bowel incontinence, including:

Damage or injury to the anal sphincter muscles or the nerves surrounding these muscles.
Anal surgery for another condition.
Certain medications, such as some antibiotics or Neurontin (an anti-seizure medication).
Improper diet.
Radiation treatment to the lower pelvic region.
Chemotherapy.
Stroke.
Conditions associated with chronic diarrhea or constipation.
Systemic (whole-body) diseases such as diabetes or scleroderma.
Spinal cord damage.

What Can I Do if I Have Bowel Incontinence?

See your doctor if you have bowel incontinence. Tests to determine the cause for incontinence can be completed during an outpatient appointment and are not painful.
Once these tests have confirmed the cause of your incontinence, your doctor can make specific recommendations for treatment, many of which do not require surgery.
No matter how serious the problem seems, incontinence is a condition that can be significantly helped and, in most cases, cured.

How Is Bowel Incontinence Diagnosed?

Endosonography, also called rectal ultrasound, makes it possible to view the anal sphincter muscles and precisely identify abnormalities. Ultrasound can be used to locate the exact position of a tear in a muscle, even before bowel incontinence becomes a problem.
Other procedures to diagnose bowel incontinence that may be used include:

Flexible sigmoidoscopy. By using a thin, flexible lighted tube called an endoscope, your doctor can examine the lining of the final third of the lower digestive tract.
Manometry. This test measures the pressure and strength of the anal muscles and can determine if they are too weak to function properly.
Nerve studies. These tests check for nerve damage to determine if the nerves that communicate with the sphincter muscles are working properly.
MRI. Magnetic resonance imaging can help identify areas of weakness in the sphincter muscles.

How Is Bowel Incontinence Treated?

Once the underlying cause of bowel incontinence has been identified, most people with this condition can be cured or the condition can be significantly improved. However, the method of treatment depends on the cause of the incontinence. Sometimes simple changes in diet or eliminating certain medications can be effective in helping patients regain bowel control. More frequently, treatment involves a combination of medication, biofeedback, and exercise.

Medication. Sometimes taking medications to change the consistency of the stool can provide relief, since a person can usually control stool better when it is firm rather than loose or liquid. Over-the-counter anti-diarrheal medications may include Imodium, and prescription medications may include Lomotil.
Biofeedback. Biofeedback training for bowel incontinence involves putting a pressure probe in the anus or a sensing electrode on the skin. These devices are attached to a visual or sound display to tell the patient when the proper anal muscles are being used. Biofeedback helps a patient improve the strength and coordination of the anal muscles that help control bowel movements, as well as heightens the sensation related to the rectum filling with stool.
Exercise. Muscle-strengthening exercises (called Kegel exercises or pelvic floor exercises) can be very helpful in treating bowel incontinence. To do Kegel exercises contract the muscles of the anus, buttocks, and pelvis and then hold as hard as possible for a slow count of five and then relax. Imagine you are trying to stop the flow of stool and urine or trying not to pass gas. A series of 30 of these exercises should be done three times daily. In a few weeks, the pelvic floor muscles will be stronger and often the incontinence improves or resolves.
Surgery. Patients who continue to experience bowel incontinence despite other treatments may require surgery to regain control. Surgery may especially be needed for patients who have experienced anal muscle injuries (as can occur during childbirth).

What Surgical Procedures Are Used to Treat Bowel Incontinence?

Surgical options for bowel incontinence include:

Sphincteroplasty. Rectal sphincter repair is the most common procedure used to correct a defect in the sphincter muscles. There are two anal muscles that control bowel movements, similar to two round doughnuts, one inside the other. If a defect exists in the complete circle of muscle, the problem can be corrected with this surgery. During the sphincteroplasty, the two ends of the muscle are cut and overlapped onto one another, then sewn in place to restore the complete circle of muscle.
Muscle transposition. During this procedure gluteal (buttock) or gracilis (inner thigh) muscles are used to encircle and strengthen the anal canal. When the inner thigh muscle is used, pacemaker-like electrodes are implanted into the grafted muscle to train it to remain contracted. When the buttock muscle is used, the lower portion of this muscle is freed from the tailbone region and wrapped around the anus to construct a new anus. The buttock muscle transposition does not require the use of a pacemaker. This procedure is an option for the small percentage of patients whose condition cannot be successfully treated with sphincteroplasty.
Colostomy. In rare and very difficult cases, the only alternative may be a (colostomy, a surgically created opening in the abdominal wall through which the colon passes, and where a bag is fitted to collect stool.

If conservative treatment or surgical repair of the anal sphincter fails to improve a patient's situation, an artificial bowel sphincter may be an option. The Acticon Neosphincter is a circular device implanted around the anus. The device can be inflated like a balloon to prevent the passage of stool. When a person has to move the bowels, the plastic ring can be deflated for stool to pass through.

Can Bowel Incontinence Be Prevented?

Since bowel incontinence in women is often caused by anal muscle or nerve damage that occurred during childbirth, prevention is not always possible. However, if the use of forceps can be avoided during childbirth, the period of labor not prolonged and the baby not delivered too rapidly, injury to the pelvic muscles and nerves can be avoided.
Also, chronic constipation may result in incontinence. Getting sufficient water, fiber, and exercise can be effective in treating constipation.

SOURCES:
National Digestive Diseases Information Clearinghouse.
Food and Drug Administration.
Medicinenet.com.
Reviewed by Venkat Mohan, MD on September 13, 2008

Portions of this page © Cleveland Clinic 2008

Heartburn and Gastroesophageal Reflux Disease (GERD)

2012-03-16T01:49:00.000-07:00

Heartburn Facts

Despite its name, heartburn has nothing to do with the heart (although some of the symptoms are similar to a heart attack). Heartburn is an irritation of the esophagus caused by acid that refluxes (comes up) from the stomach. Heartburn is also a symptom of more serious gastroesophageal reflux disease, or GERD.
When swallowing, food passes down the throat and through the esophagus to the stomach. Normally, a muscular valve called the lower esophageal sphincter (LES) opens to allow food into the stomach (or to permit belching); then it closes again. Then the stomach releases strong acids to help break down the food. But if the lower esophageal sphincter opens too often or does not close tight enough, stomach acid can reflux or seep back into the esophagus, damaging it and causing the burning sensation we know as heartburn.
Not only can stomach acid in the esophagus cause heartburn, but it can also cause ulcers, strictures (narrowing) of the esophagus, and cancer of the esophagus.
Most people have felt heartburn at one time or another. In fact, the American Gastroenterological Association reports that more than 60 million Americans experience heartburn/GERD symptoms at least once each month. Though uncomfortable, heartburn does not usually pose a serious health problem for most people.
However, if heartburn symptoms occur frequently and persistently, it may be a sign of a more serious problem, such as gastroesophageal reflux disease (GERD). GERD is a chronic reflux of acid into the esophagus. Left untreated, GERD can cause a host of complications, including esophagitis, esophageal ulcers, hoarseness, chronic pulmonary disease, and Barrett's esophagus (a change in the lining of the esophagus that increases the risk of developing cancer of the esophagus).

Heartburn Symptoms

Heartburn has several symptoms, including:

A burning feeling in the chest just behind the breastbone that occurs after eating and lasts a few minutes to several hours.
Chest pain, especially after bending over, lying down, or eating.
Burning in the throat -- or hot, sour, acidic, or salty-tasting fluid at the back of the throat.
Difficulty swallowing.
Feeling of food "sticking" in the middle of the chest or throat.

Reporting these symptoms to your doctor is usually all that is needed for your doctor to diagnose heartburn. However, your doctor may perform special tests such as endoscopy or pH monitoring to determine the severity of your problem or to monitor your treatment.

Heartburn Causes

Various lifestyle and dietary factors can contribute to heartburn by relaxing the lower esophageal sphincter and allowing it to open, increasing the amount of acid in the stomach, increasing stomach pressure, or by making the esophagus more sensitive to harsh acids. These factors include:

Dietary Habits

Eating large portions.
Eating certain foods, including onions, chocolate, peppermint, high-fat or spicy foods, citrus fruits, garlic, and tomatoes or tomato-based products.
Drinking certain beverages, including citrus juices, alcohol, caffeinated drinks, and carbonated drinks.
Eating before bedtime.

Lifestyle Habits

Being overweight
Smoking
Wearing tight-fitting clothing or belts
Lying down or bending over, especially after eating
Stress

Medical Causes

Pregnancy.
Bulging of part of the stomach into the chest cavity, also called hiatal hernia.
GERD.
Taking certain medications, especially some antibiotics and aspirin.

Heartburn Treatment

Treating heartburn requires adjustments to your lifestyle, medications, and possibly surgery if your heartburn is due to GERD or a hiatal hernia.

Tips to Alleviate Heartburn Symptoms

Raise the head of your bed about 6 inches to allow gravity to help keep the stomach's contents in the stomach. (Do not use piles of pillows because this puts your body into a bent position that actually aggravates the condition by increasing pressure on the abdomen. Instead, put books under the legs of the bed to raise it up.)
Eat meals at least three to four hours before lying down and avoid bedtime snacks.
Eat smaller meals.
Maintain a healthy weight to eliminate unnecessary intra-abdominal pressure caused by extra pounds.
Limit consumption of fatty foods, chocolate, peppermint, coffee, tea, colas, and alcohol -- all of which can relax the lower esophageal sphincter -- and tomatoes and citrus fruits or juices, which contribute additional acid that can irritate the esophagus.
Give up smoking, which also relaxes the lower esophageal sphincter.
Wear loose belts and clothing.

Heartburn can be treated with medicine. Medicines used to treat heartburn can range from over-the-counter remedies to medicine requiring a doctor's prescription.

Over-the-Counter Heartburn Treatments

Antacids. Antacids neutralize excess stomach acid to relieve heartburn, sour stomach, acid indigestion, and stomach upset. They are also occasionally recommended to help relieve the pain of ulcers. Some antacids also contain simethicone, an ingredient that helps eliminate excess gas. Examples of antacids include: Tums, Rolaids, and Maalox. You should take antacids exactly as directed by your doctor, or according to the manufacturer's directions. If you are using the tablets, chew them well before swallowing for faster relief. Serious side effects can occur with an overdose or overuse of antacids. Side effects include constipation, diarrhea, change in color of bowel movements and stomach cramps.
Acid Blockers. These medicines relieve heartburn, acid indigestion, and sour stomach, and are available without a prescription. Pepcid AC, Tagamet HB, Zantac 75, Axid AR, and Prilosec OTC are examples of over-the-counter acid blockers. Acid blockers work by reducing the production of stomach acid. Take these medications according to the directions on the package, or as advised by your doctor. Possible serious side effects that need to be reported to your doctor right away include confusion, chest tightness, bleeding, sore throat, fever, irregular heartbeat, weakness, and unusual fatigue. Other less serious side effects include mild headache, dizziness and diarrhea, which are usually temporary and will likely go away on their own.

People who have more severe heartburn symptoms that aren't relieved with these medications or who have been using these drugs for more than two weeks should contact their doctor. They may need medicine only obtained with a doctor's prescription.

Prescription Heartburn Treatments

H2 Blockers. Histamine-2 (H2) blockers such as Pepcid, Tagamet, Zantac, and Axid work by reducing the production of stomach acid. The prescription forms of these medications (which usually contain higher doses than the over-the-counter versions) can generally relieve heartburn and treat GERD. They also may be used for other conditions as determined by your doctor.
Proton Pump Inhibitors. Depending on the source of your problem, your doctor can prescribe medications that block acid production more effectively than the H2 blockers, namely the family of medications doctors call proton pump inhibitors, or PPIs for short. They include: Prilosec, Prevacid, Aciphex, Protonix, and Nexium. Another PPI product combines Prilosec with sodium bicarbonate (Zegerid).
Promotility Agents. Promotility agents work by speeding up digestion, which prevents acid from staying in the stomach too long, and strengthening the lower esophageal sphincter, reducing reflux back up into the esophagus. Reglan is a promotility agent occasionally used to treat heartburn associated with GERD. The side effects of Reglan may include drowsiness, fatigue, diarrhea, restlessness, and movement problems. Another promotility agent, Propulsid, was removed from the market in 2000 because it caused serious heart arrythmias (abnormal heart beat) in some people.

Most patients are successfully treated with these medications. Only a few people need surgery to correct the disorder.

When Is Heartburn Surgery Necessary?

Surgery for GERD may become necessary:

When medical or drug treatment has failed to control symptoms.
When the sphincter muscle is unable to work properly.
When esophageal cancer develops from chronic GERD.

SOURCES: American Gastroenterological Association.
International Foundation for Functional Gastrointestinal Disorders.
National Digestive Diseases Information Clearinghouse.
Medicinenet.com

Pregnancy: Eating Right While Pregnant

2012-03-16T01:46:00.000-07:00

Healthy Pregnancy Introduction

Eat this. Don't eat that. Do this. Don't do that. Pregnant women are bombarded with dos and don'ts. Here's help to keep it all straight.

Eating For Two

Eating healthy foods is more important now than ever! You need more protein, iron, calcium, and folic acid than you did before pregnancy. You also need more calories. But "eating for two" doesn't mean eating twice as much. Rather, it means that the foods you eat are the main source of nutrients for your baby. Sensible, balanced meals combined with regular physical fitness is still the best recipe for good health during your pregnancy.
Weight Gain
The amount of weight you should gain during pregnancy depends on your body mass index (BMI) before you became pregnant. The Institute of Medicine provides these guidelines:

If you were at a normal weight before pregnancy, you should gain about 25 to 30 pounds.
If you were underweight before pregnancy, you should gain between 28 and 40 pounds.
If you were overweight before pregnancy, you should gain between 15 and 25 pounds.
If you were obese before pregnancy, you should gain between 11 and 20 pounds.

Check with your doctor to find out how much weight gain during pregnancy is healthy for you.
You should gain weight gradually during your pregnancy, with most of the weight gained in the last trimester. Generally, doctors suggest women gain weight at the following rate:

2 to 4 pounds total during the first trimester
3 to 4 pounds per month for the second and third trimesters

Recent research shows that women who gain more than the recommended amount during pregnancy and who fail to lose this weight within six months after giving birth are at much higher risk of being obese nearly 10 years later. Findings from another large study suggest that gaining more weight than the recommended amount during pregnancy may raise your child's odds of being overweight in the future. If you find that you are gaining weight too quickly, try to cut back on foods with added sugars and solid fats. If you are not gaining enough weight, you can eat a little more from each food group.
Calorie Needs
Your calorie needs will depend on your weight gain goals. Most women need 300 calories a day more during at least the last 6 months of pregnancy than they do pre-pregnancy. Keep in mind that not all calories are equal. Your baby needs healthy foods that are packed with nutrients — not "empty calories" such as those found in soft drinks, candies, and desserts.
Although you want to be careful not to eat more than you need for a healthy pregnancy, make sure not to restrict your diet during pregnancy either. If you don't get the calories you need, your baby might not get the right amounts of protein, vitamins, and minerals. Low-calorie diets can break down a pregnant woman's stored fat. This can cause your body to make substances called ketones. Ketones can be found in the mother's blood and urine and are a sign of starvation. Constant production of ketones can result in a child with mental deficiencies.
Foods Good for Mom and Baby
A pregnant woman needs more of many important vitamins, minerals, and nutrients than she did before pregnancy. Making healthy food choices every day will help you give your baby what he or she needs to develop. The MyPyramid for Pregnant and Breastfeeding Women can show you what to eat as well as how much you need to eat from each food group based on your pre-pregnancy BMI and activity level. Use your personal MyPyramid plan to guide your daily food choices. Here are some foods to choose often:

Grains-fortified, cooked or ready-to-eat cereals; wheat germ
Vegetables-carrots, sweet potatoes, pumpkin, spinach, cooked greens, winter squash, tomatoes, red pepper
Fruits-cantaloupe, honeydew melon, mangoes, prunes or prune juice, bananas, apricots, oranges or orange juice, grapefruit, avocado
Dairy-nonfat or low-fat yogurt; nonfat milk (skim milk); low-fat milk (1% milk)
Meat and beans-cooked dried beans and peas; nuts and seeds; lean beef, lamb, and pork; shrimp, clams, oysters, and crab; cod, salmon, polluck, and catfish

Talk to your doctor if you have special diet needs for these reasons:

Diabetes - Make sure you review your meal plan and insulin needs with your doctor. High blood glucose levels can be harmful to your baby.
Lactose intolerance - Find out about low-lactose or reduced-lactose products and calcium supplements to ensure you are getting the calcium you need.
Vegetarian - Ensure that you are eating enough protein, iron, vitamin B12, and vitamin D.
PKU - Keep good control of phenylalanine levels in your diet.

Food Safety
Most foods are safe for pregnant women and their babies. But you will need to use caution or avoid eating certain foods. Follow these guidelines:
Clean, handle, cook, and chill food properly to prevent food-borne illness, including listeria and toxoplasmosis.

Wash hands with soap after touching soil or raw meat.
Keep raw meats, poultry, and seafood from touching other foods or surfaces.
Cook meat completely.
Wash produce before eating.
Wash cooking utensils with hot, soapy water.

Do not eat:

Refrigerated smoked seafood like whitefish, salmon, and mackerel
Hot dogs or deli meats unless steaming hot
Refrigerated meat spreads
Unpasteurized milk or juices
Shark, swordfish, king mackerel, or tile fish (also called golden or white snapper); these fish have high levels of mercury.
More than 6 ounces per week of white (albacore) tuna
Herbs and plants used as medicines without your doctor's okay. The safety of herbal and plant therapies isn't always known. Some herbs and plants might be harmful during pregnancy, such as bitter melon (karela), noni juice, and unripe papaya.
Raw sprouts of any kind (including alfalfa, clover, radish, and mung bean)

Fish Facts
Fish and shellfish are a great source of protein and heart-healthy omega-3 fatty acids. But pregnant women shout not eat certain kinds of fish because they contain high levels of a type of mercury that is harmful to developing babies.

Do NOT eat any shark, swordfish, king mackerel, or tile fish (also called golden or white snapper) because these fish have high levels of mercury.
Do not eat more than six ounces of "white" or "albacore" tuna or tuna steak each week.

You can safely eat up to 12 ounces per week (about 2 meals) of a variety of cooked fish.
Vitamins and Minerals
In addition to making healthy food choices, ask your doctor about taking a prenatal vitamin and mineral supplement every day to be sure you are getting enough of the nutrients your baby needs. You also can check the label on the foods you buy to see how much of a certain nutrient the product contains. Women who are pregnant need more of these nutrients than women who are not pregnant:

Nutrient	How Much Pregnant Women Need Each Day
Folic acid	400 to 800 micrograms (mcg) (.04 to .08 mg) in the early stages of pregnancy, which is why all women who are capable of pregnancy should take a daily multivitamin that contains 400 to 800 mcg of folic acid. Pregnant women should continue taking folic acid throughout pregnancy.
Iron	27 milligrams (mg)
Calcium	1,000 milligrams (mg); 1,300 mg if 18 or younger
Vitamin A	770 micrograms (mcg); 750 mcg if 18 or younger
Vitamin B12	2.6 micrograms (mcg)

Women who are pregnant also need to be sure to get enough vitamin D. The current recommendation for all adults under 50 (including pregnant women) is 5 micrograms (mcg) of vitamin D each day. But many health experts don't think this is enough. Ask your doctor how much vitamin D you need each day. Because vitamin D is important to your unborn baby's development, your doctor might want to measure your vitamin D levels to be sure you are getting enough.
Keep in mind that taking too much of a supplement can be harmful. For example, too much of the nutrient vitamin A can cause birth defects. For this reason, only take vitamins and mineral supplements that your doctor recommends.
Don't Forget Fluids
All of your body's systems need water. When you are pregnant, your body needs even more water to stay hydrated and support the life inside you. Water also helps prevent constipation, hemorrhoids, excessive swelling, and urinary tract or bladder infections. Not getting enough water can lead to premature or early labor.
Your body gets the water it needs through the fluids you drink and the foods you eat. How much fluid you need to drink each day depends on many factors, such as your activity level, the weather, and your size. Your body needs more fluids when it is hot and when you are physically active. It also needs more water if you have a fever or if you are vomiting or have diarrhea.
The Institute of Medicine recommends that pregnant women drink about 10 cups of fluids daily. Water, juices, coffee, tea, and soft drinks all count toward your fluid needs. But keep in mind that some beverages are high in sugar and "empty" calories. A good way to tell if your fluid intake is okay is if your urine is pale yellow or colorless and you rarely feel thirsty. Thirst is a sign that your body is on its way to dehydration. Don't wait until you feel thirsty to drink.
Alcohol
There is no known safe amount of alcohol a woman can drink while pregnant. When you are pregnant and you drink beer, wine, hard liquor, or other alcoholic beverages, alcohol gets into your blood. The alcohol in your blood gets into your baby's body through the umbilical cord. Alcohol can slow down the baby's growth, affect the baby's brain, and cause birth defects.
Find out more about the dangers of drinking alcohol during pregnancy in our section on Substance Abuse.
Caffeine
Small amounts of caffeine (about one 12-ounce cup of coffee a day) appear to be safe during pregnancy. Some studies have shown a link between higher amounts of caffeine and miscarriage and preterm birth. But there is no solid proof that caffeine causes these problems. The effects of too much caffeine are unclear. Ask your doctor whether drinking a limited amount of caffeine is okay for you.
Cravings
Many women have strong desires for specific foods during pregnancy. The desire for "pickles and ice cream" and other cravings might be caused by changes in nutritional needs during pregnancy. The fetus needs nourishment. And a woman's body absorbs and processes nutrients differently while pregnant. These changes help ensure normal development of the baby and fill the demands of breastfeeding once the baby is born.
Some women crave nonfood items such as clay, ice, laundry starch, or cornstarch. A desire to eat nonfood items is called pica (PYE-KUH). Eating nonfood items can be harmful to your pregnancy. Talk to your doctor if you have these urges.

Keeping Fit

Fitness goes hand in hand with eating right to maintain your physical health and well-being during pregnancy. Pregnant or not, physical fitness helps keep the heart, bones, and mind healthy. Healthy pregnant women should get at least 2 hours and 30 minutes of moderate-intensity aerobic activity a week. It's best to spread your workouts throughout the week. If you regularly engage in vigorous-intensity aerobic activity or high amounts of activity, you can keep up your activity level as long as your health doesn't change and you talk to your doctor about your activity level throughout your pregnancy.
Special benefits of physical activity during pregnancy:

Exercise can ease and prevent aches and pains of pregnancy including constipation, varicose veins, backaches, and exhaustion.
Active women seem to be better prepared for labor and delivery and recover more quickly.
Exercise may lower the risk of preeclampsia and gestational diabetes during pregnancy.
Fit women have an easier time getting back to a healthy weight after delivery.
Regular exercise may improve sleep during pregnancy.
Staying active can protect your emotional health. Pregnant women who exercise seem to have better self-esteem and a lower risk of depression and anxiety.
Results from a recent, large study suggest that women who are physically active during pregnancy may lower their chances of preterm delivery.

Getting Started
For most healthy moms-to-be who do not have any pregnancy-related problems, exercise is a safe and valuable habit. Even so, talk to your doctor or midwife before exercising during pregnancy. She or he will be able to suggest a fitness plan that is safe for you. Getting a doctor's advice before starting a fitness routine is important for both inactive women and women who exercised before pregnancy.
If you have one of these conditions, your doctor will advise you not to exercise:

Risk factors for preterm labor
Vaginal bleeding
Premature rupture of membranes (when your water breaks early, before labor)

Best Activity for Moms-to-be
Low-impact activities at a moderate level of effort are comfortable and enjoyable for many pregnant women. Walking, swimming, dancing, cycling, and low-impact aerobics are some examples. These sports also are easy to take up, even if you are new to physical fitness.
Some higher intensity sports are safe for some pregnant women who were already doing them before becoming pregnant. If you jog, play racquet sports, or lift weights, you may continue with your doctor's okay.
Keep these points in mind when choosing a fitness plan:

Avoid activities in which you can get hit in the abdomen like kickboxing, soccer, basketball, or ice hockey.
Steer clear of activities in which you can fall like horseback riding, downhill skiing, and gymnastics.
Do not scuba dive during pregnancy. Scuba diving can create gas bubbles in your baby's blood that can cause many health problems.

Tips for Safe and Healthy Physical Activity
Follow these tips for safe and healthy fitness:

When you exercise, start slowly, progress gradually, and cool down slowly.
You should be able to talk while exercising. If not, you may be overdoing it.
Take frequent breaks.
Don't exercise on your back after the first trimester. This can put too much pressure on an important vein and limit blood flow to the baby.
Avoid jerky, bouncing, and high-impact movements. Connective tissues stretch much more easily during pregnancy. So these types of movements put you at risk of joint injury.
Be careful not to lose your balance. As your baby grows, your center of gravity shifts making you more prone to falls. For this reason, activities like jogging, using a bicycle, or playing racquet sports might be riskier as you near the third trimester.
Don't exercise at high altitudes (more than 6,000 feet). It can prevent your baby from getting enough oxygen.
Make sure you drink lots of fluids before, during, and after exercising.
Do not workout in extreme heat or humidity.
If you feel uncomfortable, short of breath, or tired, take a break and take it easier when you exercise again.

Stop exercising and call your doctor as soon as possible if you have any of the following:

Dizziness
Headache
Chest pain
Calf pain or swelling
Abdominal pain
Blurred vision
Fluid leaking from the vagina
Vaginal bleeding
Less fetal movement
Contractions

Work Out Your Pelvic Floor (Kegel Exercises)
Your pelvic floor muscles support the rectum, vagina, and urethra in the pelvis. Toning these muscles with Kegel exercises will help you push during delivery and recover from birth. It also will help control bladder leakage and lower your chance of getting hemorrhoids.
Pelvic muscles are the same ones used to stop the flow of urine. Still, it can be hard to find the right muscles to squeeze. You can be sure you are exercising the right muscles if when you squeeze them you stop urinating. Or you can put a finger into the vagina and squeeze. If you feel pressure around the finger, you've found the pelvic floor muscles. Try not to tighten your stomach, legs, or other muscles.
Kegel Exercises

Tighten the pelvic floor muscles for a count of 3, then relax for a count of 3.
Repeat 10 to 15 times, 3 times a day.
Start Kegel exercises lying down. This is the easiest position. When your muscles get stronger, you can do Kegel exercises sitting or standing as you like.

Oral Health

Before you become pregnant, it is best to have dental checkups every 6 months to keep your teeth and gums healthy. If you are pregnant and have not had regular checkups, consider the following:

Have a complete oral exam early in your pregnancy. Because you are pregnant, you might not receive routine x-rays. But if you must have x-rays for a dental problem needing treatment, the health risk to your unborn baby is small.
Dental treatment during pregnancy is safe. The best time for treatment is between the 14th and 20th weeks. During the last months of pregnancy, you might be uncomfortable sitting in a dental chair.
Do not avoid necessary dental treatments — you may risk your and your baby's health.
Use good oral hygiene to control your risk of gum diseases. Pregnant women may have changes in taste and develop red, swollen gums that bleed easily. This condition is called pregnancy gingivitis (jin-juh-VYT-uhss). It can be caused by both poor oral hygiene and higher hormone levels during pregnancy. Until recently, it was thought that having gum disease could raise your risk of having a low-birth-weight baby. Researchers have not been able to confirm this link, but some research is still under way to learn more.

After you give birth, maintain good oral hygiene to protect your baby's oral health. Bacteria that cause cavities can transfer from you to your child by:

A kiss on the mouth
Letting your baby put her fingers in your mouth
Tasting food on your baby's spoon
Testing the temperature of a baby bottle with your mouth

Using Medicine and Herbs

You and your baby are connected. So medicines you use, including over-the counter, herbal, and prescription drugs or supplements, might get into your baby's system too. Many medicines and herbs are known to cause problems during pregnancy, including birth defects. For some medicines, we don't know that much about how they might affect pregnancy or the developing fetus. This is because medicines are rarely tested on pregnant women for fear of harming the fetus.
Mothers-to-be might wonder if it's safe to use medicines during pregnancy. There is no clear-cut answer to this question. Your doctor can help you make the choice whether to use a medicine. Labels on prescription and over-the-counter drugs have information to help you and your doctor make this choice. In the future, a new prescription drug label will make it easier for women and their doctors to weigh the benefits and risks of using prescription medicines during pregnancy.
Always speak with your doctor before you start or stop any medicine. Not using medicine that you need may be more harmful to you and your baby than using the medicine.
Weighing Benefits and Risks
When deciding whether or not to use a medicine in pregnancy, you and your doctor need to talk about the medicine's benefits and the risks.

Benefits-what are the good things the medicine can do for me and my growing baby?
Risks-what are the ways the medicine might harm me or my growing baby?

There may be times during pregnancy when using medicine is a choice. For example, if you get a cold, you may decide to "live with" your stuffy nose instead of using the "stuffy nose" medicine you use when you are not pregnant.
Other times during pregnancy, using medicine is not a choice — it is needed. For example, you might need to use medicine to control an existing health problem like asthma, diabetes, depression, or seizures. Or, you might need a medicine for a few days, such as an antibiotic to treat a bladder infection or strep throat. Also, some women have a pregnancy problem that needs medicine treatment. These problems include severe nausea and vomiting, earlier pregnancy losses, or preterm labor.
Using Herbal or Dietary Supplements and Other "Natural" Products
You might think herbs are safe because they are "natural." But, except for some vitamins, little is known about using herbal or dietary supplements while pregnant. Some herbal remedy labels claim they will help with pregnancy. But, most often there are no good studies to show if these claims are true or if the herb can cause harm to you or your baby. Also, some herbs that are safe when used in small amounts as food might be harmful when used in large amounts as medicines. So, talk with your doctor before using any herbal or dietary supplement or natural product. These products may contain things that could harm you or your growing baby.

Having Sex

Unless your doctor tells you otherwise, sex is safe. You may find that your interest in sex changes during pregnancy. Talk to your partner about other positions if the way you usually have sex is awkward or no longer feels good. Call your doctor if sex causes:

Pain
Vaginal bleeding
Fluid leakage

Travel

Everyday life doesn't stop once you are pregnant. Most healthy pregnant women are able to continue with their usual routine and activity level. That means going to work, running errands, and for some, traveling away from home. To take care of yourself and help keep your baby safe, consider these points before taking a long trip or traveling far from home:
Buckle up-Wearing a seatbelt during car and air travel is safe while pregnant. The lap strap should go under your belly, across your hips. The shoulder strap should go between your breasts and to the side of your belly. Make sure it fits snugly.

Talk to your doctor before making any travel decisions that will take you far from home. Ask if any health conditions you might have makes travel during pregnancy unsafe. Also consider the destination. Is the food and water safe? Will you need immunizations before you go? Is there good medical care available in the event of an emergency? Will your health insurance cover medical care at your destination? Also, avoid traveling to very high altitudes (12,000 feet).
Bring a copy of your medical record and find out about medical care at your destination so you will be prepared in the event of an emergency.
Avoid sitting for long periods during car or air travel. Prolonged sitting can affect blood flow in your legs. Take frequent, 10 minute breaks while traveling by car to walk and stretch. Stand up, and move your legs often during air travel. Wearing support pantyhose also can help blood flow.
If you suspect a problem with your pregnancy during your trip, don't wait until you come home to see your doctor. Seek medical care right away.

Environmental Risks

The environment is everything around us wherever we are — at home, at work, or outdoors. While you don't need to worry about every little thing you breathe in or eat, it's smart to avoid exposure to substances that might put your pregnancy or unborn baby's health at risk.
During pregnancy, avoid exposure to:

Lead – found in some water and paints, mainly in homes built before 1978
Mercury – the harmful form is found mainly in large fish
Arsenic – high levels can be found in some well water
Pesticides – both household products and agricultural pesticides
Solvents – such as degreasers and paint strippers and thinners
Cigarette smoke

Keep in mind: We don't know how much exposure can lead to problems, such as miscarriage or birth defects. That is why it's best to avoid or limit your exposure as much as possible. Here are some simple, day-to-day precautions you can take:

Clean in only well-ventilated spaces. Open the windows or turn on a fan.
Check product labels for warnings for pregnant women and follow instructions for safe use.
Do not clean the inside of an oven while pregnant.
Leave the house if paint is being used, and don't return until the fumes are gone.

If you are exposed to chemicals in the workplace, talk to your doctor and your employer about what you can do lower your exposure. Certain industries, such as dry cleaning, manufacturing, printing, and agriculture, involve use of toxins that could be harmful. If you are concerned about the safety of your drinking water, call your health department or water supplier to ask about the quality of your tap water or how to have your water tested. Or, call the Environmental Protection Agency's Safe Drinking Water Hotline at (800) 426-4791. Don't assume that bottled water is better or safer. Usually, bottle water offers no health benefits over tap water.

Quitting Smoking

Smoking cigarettes is very harmful to your health and could also affect the health of your baby. Not only does smoking cause cancer and heart disease in people who smoke, a recent large study confirmed that smoking during pregnancy increases the risk of low birth weight. Low-birth-weight babies are at higher risk of health problems shortly after birth. Also, some studies have linked low birth weight with a higher risk of health problems later in life, such as high blood pressure and diabetes. Women who smoke during pregnancy are more likely than other women to have a miscarriage and to have a baby born with cleft lip or palate, types of birth defects. Also, mothers who smoke during or after pregnancy put their babies at greater risk of sudden infant death syndrome (SIDS).
Mothers who smoke have many reasons to quit smoking. Take care of your health and your unborn baby's health by asking your doctor for help quitting smoking. Quitting smoking is hard, but you can do it with help!

Substance Abuse

Using alcohol and illegal drugs during pregnancy threatens the health of your unborn baby. So does using legal drugs in an inappropriate way. When you use alcohol or drugs, the chemicals you ingest or breathe into your lungs cross the placenta and enter your baby. This puts your baby at risk for such problems as stillbirth, low birth weight, birth defects, behavioral problems, and developmental delays.
Alcohol
When you drink alcohol, so does your baby. Pregnant women should not drink alcohol to eliminate the chance of giving birth to a baby with fetal alcohol spectrum disorder (FASD). FASD involves a range of harmful effects that can occur when a fetus is exposed to alcohol. The effects can be mild to severe. Children born with a severe form of FASD can have abnormal facial features, severe learning disabilities, behavioral problems, and other problems.
You might think a drink now and then won't hurt your baby. But we don't know how much alcohol it takes to cause harm. We do know that the risk of FASD, and the likely severity, goes up with the amount of alcohol consumed during pregnancy. Also, damage from alcohol can occur in the earliest stages of pregnancy — often before a woman knows she is pregnant. For this reason, women who may become pregnant also should not drink.
Illegal Drugs
Many women who use illegal drugs also use tobacco and alcohol. So, it's not always easy to tell the effects of one drug from that of alcohol, tobacco, or other drugs. We do know that using illegal drugs during pregnancy is very dangerous. Babies born to women who use drugs such as cocaine, heroine, and methamphetamine are likely to be born addicted and must go through withdrawal. Mothers who inject drugs are at higher risk of getting HIV, which can be passed to an unborn baby. Some studies suggest that the effects of drug use during pregnancy might not be seen until later in childhood.
Getting Help for Alcohol or Drug Use
If you drink alcohol or use drugs and cannot quit, talk to your doctor right away. Treatment programs can help pregnant women with addiction and abuse. To find help near you, go to the Substance Abuse Treatment Facility Locator. You can quit using and give your baby a good start to life.

Abusive Relationships

It's hard to be excited about the new life growing inside of you if you're afraid of your partner. Abuse from a partner can begin or increase during pregnancy and can harm you and your unborn baby. Women who are abused often don't get the prenatal care their babies need. Abuse from a partner also can lead to preterm birth and low-birth-weight babies, stillbirth and newborn death, and homicide. If you are abused, you might turn to alcohol, cigarettes, or drugs to help you cope. This can be even more harmful to you and your baby.
You may think that a new baby will change your situation for the better. But the cycle of abuse is complex, and a baby introduces new stress to people and relationships. Now is a good time to think about your safety and the safety and wellbeing of your baby. About 50 percent of men who abuse their wives also abuse their children. Think about the home environment you want for your baby. Studies show that children who witness or experience violence at home may have long-term physical, emotional, and social problems. They are also more likely to experience or commit violence themselves in the future.
Prenatal exams offer a good chance to reach out for help. It's possible to take control and leave an abusive partner. But for your and your baby's safety, talk to your doctor first. Let motherhood prompt you to take action now.
If you're a victim of abuse or violence at the hands of someone you know or love, or you are recovering from an assault by a stranger, you and your baby can get immediate help and support.
The National Domestic Violence Hotline can be reached 24 hours a day, 7 days a week at 800-799-SAFE (7233) and 800-787-3224 (TTY). Spanish speakers are available. When you call, you will first hear a recording and may have to hold. Hotline staff offer crisis intervention and referrals. If requested, they connect women to shelters and can send out written information.
The National Sexual Assault Hotline can be reached 24 hours a day, 7 days a week at 800-656-4673. When you call, you will hear a menu and can choose #1 to talk to a counselor. You will then be connected to a counselor in your area who can help you. You can also visit the National Sexual Assault Online Hotline.

When to Call the Doctor

When you are pregnant, do not hesitate to call your doctor or midwife if something is bothering or worrying you. Sometimes physical changes can be signs of a problem.
Call your doctor or midwife as soon as you can if you:

are bleeding or leaking fluid from the vagina
have sudden or severe swelling in the face, hands, or fingers
get severe or long-lasting headaches
have discomfort, pain, or cramping in the lower abdomen
have a fever or chills
are vomiting or have persistent nausea
feel discomfort, pain, or burning with urination
have problems seeing or blurred vision
feel dizzy
suspect your baby is moving less than normal after 28 weeks of pregnancy (if you count less than 10 movements within 2 hours)
have thoughts of harming yourself or your baby

SOURCES: womenshealth.gov

Medicinenet.com.

Sexual Problems in Men

2012-03-16T01:39:00.000-07:00

Introduction

A sexual problem, or sexual dysfunction, refers to a problem during any phase of the sexual response cycle that prevents the individual or couple from experiencing satisfaction from the sexual activity. The sexual response cycle has four phases: excitement, plateau, orgasm, and resolution.
While research suggests that sexual dysfunction is common (43% of women and 31% of men report some degree of difficulty), it is a topic that many people are hesitant to discuss. Fortunately, most cases of sexual dysfunction are treatable, so it is important to share your concerns with your partner and doctor.

What Causes Sexual Problems?

Sexual dysfunction can be a result of a physical or psychological problem.

Physical causes: Many physical and/or medical conditions can cause problems with sexual function. These conditions include diabetes, heart and vascular (blood vessel) disease, neurological disorders, hormonal imbalances, chronic diseases such as kidney or liver failure, and alcoholism and drug abuse. In addition, the side effects of certain medications, including some antidepressant drugs, can affect sexual desire and function.
Psychological causes: These include work-related stress and anxiety, concern about sexual performance, marital or relationship problems, depression, feelings of guilt, and the effects of a past sexual trauma.

Who is Affected by Sexual Problems?

Both men and women are affected by sexual problems. They can occur in adults of all ages. Among those commonly affected are seniors, which may be related to a decline in health associated with aging.

How do Sexual Problems Affect Men?

The most common sexual problems in men are ejaculation disorders, erectile dysfunction, and inhibited sexual desire.

What Are Ejaculation Disorders?

There are different types of ejaculation disorders, including:

Premature ejaculation -- This refers to ejaculation that occurs before or soon after penetration.
Inhibited or retarded ejaculation -- This is when ejaculation is slow to occur.
Retrograde ejaculation -- This occurs when, at orgasm, the ejaculate is forced back into the bladder rather than through the urethra and out the end of the penis.

In some cases, premature and inhibited ejaculation are caused by a lack of attraction for a partner, past traumatic events, and psychological factors, including a strict religious background that causes the person to view sex as sinful. Premature ejaculation, the most common form of sexual dysfunction in men, often is due to nervousness over how well he will perform during sex. Certain drugs, including some antidepressants, may affect ejaculation, as can nerve damage to the spinal cord or back.
Retrograde ejaculation is common in males with diabetes who suffer from diabetic neuropathy (nerve damage). This is due to problems with the nerves in the bladder and the bladder neck that allow the ejaculate to flow backward and into the bladder. In other men, retrograde ejaculation occurs after operations on the bladder neck or prostate, or after certain abdominal operations. In addition, certain medications, particularly those used to treat mood disorders, may cause problems with ejaculation. This generally does not require treatment unless it impairs fertility.

What is Erectile Dysfunction?

Also known as impotence or ED, erectile dysfunction is defined as the inability to attain and/or maintain an erection suitable for intercourse. Causes of erectile dysfunction include diseases affecting blood flow, such as atherosclerosis (hardening of the arteries); nerve disorders; psychological factors, such as stress, depression, and performance anxiety (nervousness over his ability to sexually perform); and injury to the penis. Chronic illness, certain medications, and a condition called Peyronie's disease (scar tissue in the penis) can also cause erectile dysfunction.

What is Inhibited Sexual Desire?

Inhibited desire, or loss of libido, refers to a decrease in desire for, or interest in sexual activity. Reduced libido can result from physical or psychological factors. It has been associated with low levels of the hormone testosterone. It also may be caused by psychological problems, such as anxiety and depression; medical illnesses, such as diabetes and high blood pressure; certain medications, including some antidepressants; and relationship difficulties.

How Are Male Sexual Problems Diagnosed?

To diagnose a man's sexual problem, the doctor likely will begin with a thorough history of symptoms. He or she may order other tests to rule out any medical problems that may be contributing to the dysfunction. The doctor may refer you to other doctors, including a urologist (a doctor specializing in the urinary tract and male reproductive system), an endocrinologist (a doctor specializing in hormonal issues), a neurologist (a doctor specializing in disorders of the nervous system), sex therapists, and other counselors.

What Tests Are Used to Evaluate Sexual Problems?

Several tests can be used to evaluate the causes and extent of male sexual problems. They include:

Blood tests -- These tests are done to evaluate hormone levels.
Vascular assessment -- This involves an evaluation of the blood flow to the penis. A blockage in a blood vessel supplying blood to the penis may be contributing to erectile dysfunction.
Sensory testing -- Particularly useful in evaluating the effects of diabetic neuropathy (nerve damage), sensory testing measures the strength of nerve impulses in a particular area of the body.
Nocturnal penile tumescence and rigidity testing -- This test is used to monitor erections that occur naturally during sleep. This test can help determine if a man's erectile problems are due to physical or psychological causes.

How Is Male Sexual Dysfunction Treated?

Many cases of male sexual dysfunction can be corrected by treating the underlying physical or psychological problems. Treatment strategies may include the following:

Medical treatment -- This involves treatment of any physical problem that may be contributing to a man's sexual dysfunction.
Medications -- Medications, such as Cialis, Viagra or Levitra, may help improve sexual function in men by increasing blood flow to the penis.
Hormones -- Men with low levels of testosterone may benefit from hormone supplementation (testosterone replacement therapy).
Psychological therapy -- Therapy with a trained counselor can help a person address feelings of anxiety, fear, or guilt that may have an impact on sexual function.
Mechanical aids -- Aids such as vacuum devices and penile implants may help men with erectile dysfunction.
Education and communication -- Education about sex and sexual behaviors and responses may help a man overcome his anxieties about sexual performance. Open dialogue with your partner about your needs and concerns also helps to overcome many barriers to a healthy sex life.

Can Sexual Problems Be Cured?

The success of treatment for sexual problems depends on the underlying cause. The outlook is good for dysfunction that is related to a treatable or reversible physical condition. Mild dysfunction that is related to stress, fear, or anxiety often can be successfully treated with counseling, education, and improved communication between partners.

Can Sexual Problems be Prevented?

While sexual problems cannot be prevented, dealing with the underlying causes of the dysfunction can help you better understand and cope with the problem when it occurs. There are some things you can do to help maintain good sexual function:

Follow your doctor's treatment plan for any health conditions.
Limit your alcohol intake.
Quit smoking.
Deal with any emotional or psychological issues such as stress, depression, and anxiety. Get treatment as needed.
Increase communication with your partner.

When Should I Call My Doctor About a Sexual Problem?

Many men experience a sexual problem from time to time. However, when the problems are persistent, they can cause distress for the man and his partner, and have a negative impact on their relationship. If you consistently experience sexual function problems, see your doctor for evaluation and treatment.
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