 1 Sepsis, septic workup
 2 Spondylolysis (spinal disk)
 3 gangrene poisoning
 4 migraine headaches
 5 heartburn (reflux)
 6 Lupus
 7 blood pressure, hypertension
 8 Homosysteine
 9 Urinary incontinence
 10 Yeast infections (candida)

\1 Sepsis, septic workup

Sepsis refers to bacterial infection of the bloodstream. It means that the normal defenses of the body against overwhelming infection are breaking down and bacterial germs are loose and multiplying in the bloodstream. Once this state has arisen, the patient's chances for recovery begin to dwindle rapidly. Sepsis is a medical emergency requiring swift and decisive intervention. Septic shock and death will follow if this condition is left untreated for long. Consequences of missing sepsis are so dire, and because the early signs of sepsis may be quite subtle, physicians often perform what is referred to as the "septic workup," which means obtaining culture specimens of blood, urine, and spinal fluid (via lumbar puncture or spinal tap). While awaiting these test results, powerful antibiotics are administered intravenously in high doses until the situation is more clear - whether the patient is truly gravely infected or perhaps suffering from another illness, often viral, which is not serious. Most septic workups are performed on very young infants, because these children in particular are the most difficult to assess on clinical grounds (physical examination, history or presence of fever, and routine lab tests such as blood count). Most septic workups are false alarms, but they are a small price to pay for saving young lives.

For this reason, that the consequences of missing sepsis are so dire, and because the early signs of sepsis may be quite subtle, physicians often perform what is referred to ss the "septic workup," which eeans obtaining culture specimens of blood, urine, and spinal fluid (via lumbar puncture or spinal tap). While awaiting these test results, powerful antibiotics are administered intravenously in high doses until the situation is more clear - whether the patient is truly gravely infected or perhaps suffering from another illness, often viral, which is not serious.

Most septic workups are performed on very young infants, because these children in particular are the most diffi-cult to assess on clinical grounds (physical examination, history or presence of fever, and routine lab tests such as blood count). Most septic workups are false alarms, but they are a small price to pay for saving young lives.

Sepsis is a severe infection in the body and bloodstream that can lead to shock, a reaction caused by lack of blood flow in the body.

What is going on in the body? Sepsis can occur when a person has a severe infection. The infection may start in any part of the body, but usually starts with pneumonia (new-moan-ya), a serious inflammation in the lungs, or a urinary infection. Sepsis can also occur after an abdominal infection such as appendicitis (ah-pend-i-site-is). As the infection worsens, bacteria may enter the bloodstream. When this happens, toxins produced by the bacteria can affect the blood vessels. This causes severe low blood pressure. This is known as septic shock, and is a medical emergency. If not treated, septic shock will lead to death.

What are the signs and symptoms of the infection? Symptoms of septic shock include: ? very low blood pressure ? fast heart rate ? weak pulse ? fever ? flushing of the skin ? sweating ? changes in mental status

What are the causes and risks of the infection? Septic shock can occur with any severe infection. It is more common with severe abdominal infections or lung infections such as pneumonia. People with an immune system that is not working are especially prone to septic shock. This includes people with AIDS or those getting cancer treatment. The very young and very old are also prone to sepsis.

What can be done to prevent the infection? Preventing or treating the initial infection can prevent sepsis. Not all infections lead to sepsis.

How is the infection diagnosed? The diagnosis is based on a physical examination and a history of severe infection. Sepsis is also suspected when a person has low blood pressure and a fast heart rate. Blood cultures are done. These will often show growth of bacteria. This confirms the diagnosis.

What are the long-term effects of the infection? People with sepsis will either get rid of underlying infection or die. There are few long-term effects related to sepsis. In some cases, the brain or kidneys may be permanently damaged.

What are the risks to others? Although sepsis is caused by infections, these infections are usually not contagious.

What are the treatments for the infection? Sepsis is treated with antibiotics, fluids injected directly into the body, and medications to restore normal blood pressure. The person is usually treated in the intensive care unit of a hospital. Certain heart or lung monitors may be placed in the person to measure blood pressure and other vital signs. Some people may need a ventilator (a breathing machine) to help them breathe. Sepsis will usually improve as the infection heals. In some cases surgery, is needed to remove or drain an abscess (ab-sess) or other tissue.

What are the side effects of the treatments? Side effects depend on the medication taken. People who have surgery are at high risk.

What happens after treatment for the infection? The person is monitored to make sure blood pressure returns to normal and the sepsis resolves.

How is the infection monitored? The person will be monitored with physical examinations and blood tests. Cultures will be taken of blood, urine, or other fluids to check for continuing infection.

Septic shock; Systemic inflammatory response syndrome (SIRS)

Definition - Sepsis is a serious, severe illness caused by infection of the bloodstream. Illness is a result of toxins produced by bacteria, and the body's response to these toxins.

Causes and risks - Sepsis occurs in 2 of every 100 hospital admissions. It is a result of a bacterial infection that can originate anywhere in the body. Common sites are the kidneys (upper urinary tract infection), the liver or gall bladder, the bowel (usually seen with peritonitis), the skin (cellulitis) and the lungs (bacterial pneumonia).

Meningitis may also be accompanied by sepsis. In children, sepsis may accompany infection of the bone (osteomyelitis). In hospitalized patients, common sites of infection include intravenous lines, surgical wounds, surgical drains, and sites of skin breakdown known as decubitus ulcers or bedsores.

The infection is often confirmed by a positive blood culture, though blood cultures may be negative in individuals who have been receiving antibiotics. In sepsis, blood pressure drops resulting in shock. Major organ systems, including the kidneys, liver, lungs, and central nervous system, stop functioning normally. A change in mental status and hyperventilation may be the earliest signs of impending sepsis.

Sepsis is often life-threatening, especially in people with a weakened immune system or other medical illnesses.

Prevention Return to top

Many cases are not preventable. Awareness of risk may allow earlier detection. Symptoms Return to top

Fever or hypothermia (low body temperature) Hyperventilation Chills Shaking Warm skin Skin rash Rapid heart beat (tachycardia) Confusion or delirium Decreased urine output Signs and tests Return to top

White blood cell count that is low or high Platelet count is often low Blood culture that is positive for bacteria Blood gases that reveal acidosis Kidney function tests often become abnormal early in the course of disease This disease may also alter the results of the following tests: Peripheral smear may demonstrate a low platelet count and destruction of red blood cells Fibrin degradation products are often elevated, a condition that may be associated with a tendency to bleed

Blood differential, with immature white blood cells seen Treatment Return to top

Individuals frequently require monitoring in an intensive care unit setting. "Broad spectrum" intravenous antibiotic therapy should be initiated as soon as the diagnosis is suspected.

The number of antibiotics administered may be decreased when the results of blood cultures become available. The source of the infection should be identified if possible, which may mean further diagnostic testing. Sources such as infected intravenous lines or surgical drains can be removed, and sources such as abscesses can be surgically drained.

Supportive therapy with oxygen, intravenous fluids, and medications that increase blood pressure may be required for a good outcome. In the event of kidney failure, dialysis may be necessary, and mechanical ventilation is often required if respiratory failure occurs.

Prognosis - The death rate can be as high as 60% for people with underlying medical problems. Mortality is less (but still significant) in individuals without other medical problems.

Complications - Septic shock Impaired blood flow to vital organs (brain, heart, kidneys) Disseminated intravascular coagulation Call your health care provider if Return to top

Call your health care provider if symptoms of sepsis occur. This condition can rapidly progress to become an emergency situation.

The lethal sequelae of infection and septic shock continue to claim the lives of thousands of patients annually in intensive care units (ICU) and consume a disproportionate percentage of health care costs. Substantial hospital expenditures are directed at infection control yet the mortality rate due to infections remains unchanged and ranges up to 40% in many ICU patients with infection. Due to antibiotic overuse we are seeing the emergence of superbugs which are antibiotic resistant. In North America alone, each year more than 500,000 cases of septic shock along with a larger reported number of cases of other endotoxin related infections occur.

The basic technology for detecting infection relies on time consuming manual culture techniques. A diagnostic test to trigger, direct and monitor therapy of infection remains an unmet need in hospitals. With the development of our gram-negative diagnostic test as a rapid indicator of bacterial toxins (Endotoxin), physicians will be assisted in stratifying patients into those who are at low risk of life threatening gram-negative infection and those who require directed antibiotic or anti-mediator therapy. This diagnostic capability will permit rational and cost effective use of antibiotics and newly emerging anti-mediator therapies.

During the past year, the design and development of the gram-negative test has advanced to commercial scale production. Commencement of clinical trials at eight international recognized intensive care centers began in 2000 and are scheduled for completion this year. Submission of the pre-market approval (PMA) FDA filing in the US for the gram-negative test is targeted for later this year.

Contemporaneous with the progression of clinical trials, we have completed our manufacturing capability and are in the process of registering the facility with the FDA and Health Canada.

FDA APPROVES FIRST BIOLOGIC TREATMENT FOR SEPSIS
 FDA today approved the first biologic treatment for the most serious forms of sepsis, a life-threatening illness caused by severe infection. The new treatment is a genetically engineered version of a naturally occurring human protein, Activated Protein C, which interferes with some of the body's harmful responses to severe infection, including the formation of blood clots that can lead to organ failure and death. Eli Lilly and Co., Indianapolis, Ind., will market the product as Xigris.

"Xigris is a new treatment that helps to save the lives of patients with the most severe forms of sepsis" said FDA's Acting Principal Deputy Commissioner Bernard A. Schwetz, D.V.M., Ph.D. "While not everyone will benefit from this treatment, we believe the approval of Xigris is an important advance for the treatment of this often deadly disease."

Of about 750,000 people who get sepsis in the U.S. each year, an estimated 30% will die from it, despite treatment with intravenous antibiotics and supportive care. Patients with severe sepsis often experience failures of various systems in the body,including the circulatory system, as well as kidney failure, bleeding, and clotting.

Xigris was approved by FDA for the treatment of adult patients with severe sepsis who have an especially high risk of dying from sepsis, as measured by a scoring system based on their general health and the severity of their illness.

In a placebo-controlled, multi-center, randomized clinical trial of nearly 1700 patients, the overall mortality rate was reduced by 6%(from 31% to 25%) during the 28 day study period of the trial. Although treatment with Xigris did not lower mortality rates in patients in the study who were less severely ill, among patients at higher risk of dying, the group for whom Xigris is now indicated, mortality was reduced 13 percent (from 44% to 31%).

Because Activated Protein C interferes with blood clotting, the most serious side effect associated with Xigris therapy is bleeding, including bleeding that causes stroke. During the period of time when the drug was infused (continuously over four days), serious bleeding episodes occurred in 2.4% of patients treated with Xigris compared to 1% of patients in the placebo group. Patients at high risk of bleeding were excluded from the trial, as were severely ill patients with pre-existing conditions not related to sepsis that made them likely to die within the study period.

Xigris is contraindicated -- should not be used -- for patients who have active internal bleeding, or who are more likely to bleed because of certain medical conditions including recent strokes, recent head or spinal surgery or severe head trauma.

Because sepsis is a life-threatening condition and because treatment with Xigris comes with potentially serious risks, the benefits and risks of treatment with Xigris must be carefully weighed for each individual patient.

\2 Spondylolysis

What is degenerative disc disease? As we age, the water and protein content of the bodys cartilage changes. This change results in weaker, more fragile and thin cartilage. Because both the discs and the joints that stack the vertebrae (facet joints) are partly composed of cartilage, these areas are subject to wear and tear over time (degenerative changes). The gradual deterioration of the disc between the vertebrae is referred to as degenerative disc disease.

Degenerative Disc - Degeneration of the disc is medically referred to as spondylosis. Spondylosis can be noted on x-ray tests or MRI scanning of the spine as a narrowing of the normal "disc space" between the adjacent vertebrae.

Degeneration of the disc tissue makes theddisc more susceptible to herniation and resulting localized pain. Any level of the spine can be affected by disc degeneration. When disc degeneration affects the spine of the neck, it is referred to as cervical disc disease. When the mid-back is affected, the condition is referred to as thoracic disc disease. Disc degeneration that affects the lumbar spine is referred to as lumbago. Lumbago causes pain localized to the low back and is common in older patients. Degenerative arthritis (osteoarthritis) of the facet joints is also a cause of localized lumbar pain that can be detected with plain x-ray testing. The pain from degenerative disc or joint disease of the spine is usually treated conservatively with intermittent heat, rest, rehabilitative exercises, and medications to relieve pain, muscle spasm, and inflammation.

What are radiculopathy and sciatica? Radiculopathy refers to nerve irritation caused by damage to the disc between the vertebrae. This occurs because of degeneration ("wear and tear") of the outer ring of the disc, or because of traumatic injury, or both. Weakness of the outer ring leads to disc bulging and herniation. As a result, the central softer portion of the disc can rupture through the outer ring of the disc and abut the spinal cord or its nerves as they exit the bony spinal column.

When nerves are irritated in the neck from degenerative disc disease, the condition is referred to as cervical radiculopathy. This can lead to painful burning or tingling sensations in the arms. When nerves are irritated in the low back from degenerative disc disease, the condition is called lumbar radiculopathy and it often causes the commonly recognized "sciatica" pain that shoots down the lower extremity. This condition can be preceded by a localized low back aching. Sciatica pain can follow a "popping" sensation at onset and be accompanied by numbness and tingling. The pain commonly increases with movements at the waist and can increase with coughing or sneezing. In more severe instances, lumbar radiculopathy can be accompanied by incontinence of the bladder and/or bowels.

How is radiculopathy diagnosed? Radiculopathy is suspected when the symptoms described above are noted. The doctor can sometimes detect signs of irritated nerves during the examination. For example, increased radiating pain when the lower extremity is lifted supports the diagnosis of lumbar radiculopathy. Nerve testing (EMG/electromyogram and NCV/nerve conduction velocity) of the lower extremities can be used to detect the nerve irritation. The actual disc herniation can be detected with radiology testing, such as CAT or MRI scanning. For more info, visit the CAT Scanning and MRI Scanning forums.

How is radiculopathy treated? The treatment of radiculopathy ranges from nonsurgical (med) management to surgery. Medical management of radiculopathy includes patient education of the condition, medications to relieve pain and muscles spasm, cortisone injection around the spinal cord (epidural injection), physical therapy (heat, massage, ultrasound, electrical stimulation), and rest (not strict bed rest, but avoiding re-injury). With unrelenting pain, severe impairment of function, or incontinence (which can indicate spinal cord irritation), surgery may be necessary. The operation performed depends on the overall status of the spine, and the age and health of the patient. Procedures include removal of the herniated disc with laminotomy (a small hole in the bone of the spine surrounding the spinal cord), laminectomy (removal of the bony wall), by needle technique through the skin (percutaneous discectomy), disc- dissolving procedures (chemonucleolysis), and others.

What is bony encroachment? Any condition that results in movement or growth of the bony vertebrae of the spine can limit the space (encroachment) for the adjacent spinal cord and nerves. Causes of bony encroachment of the spinal nerves include foramenal narrowing (narrowing of the portal through which the spinal nerve passes from the spinal column, out of the spinal canal to the body), spondylolisthesis (slipping of one vertebra relative to another), and spinal stenosis (compression of the nerve roots or spinal cord by bony spurs or other soft tissues in the spinal canal).

For example, lumbar spinal nerve compression in these conditions can lead to sciatica pain which radiates down the lower extremities. Lumbar spinal stenosis can cause lower extremity pains which worsen with walking and are relieved by resting (mimicking poor circulation). Treatment of these conditions varies (depending on the severity and condition of the patient) from rest to surgical decompression by removing the bone that is compressing the nervous tissue.

Degenerative Disc Disease & Sciatica At A Glance - The discs of the spine serve as "cushions" between each vertebral segment. The discs are designed somewhat like a jelly donut. Degeneration (deterioration) of the disc makes the disc more susceptible to herniation (rupture) which can lead to localized or radiating pain. Sciatica can result from disc herniation when nerves of sensation in the low back are irritated.

Author: William C. Shiel Jr., MD, FACP, FACR 4/01.

Spondylolysis and Spondylolisthesis The most common cause of low back pain in adolescent athletes is a stress fracture in one of the bones (vertebrae) that make up the spinal column. Technically, this condition is called spondylolysis (spon-dee-low-lye-sis). It usually affects either the fourth or the fifth lumbar vertebra in the lower back.

If the stress fracture weakens the bone so much that it is unable to maintain its proper position, the vertebra can start to slip out of place. This condition is called spondylolisthesis (spon-dee-low-lis-thee-sis). In adults, spondylolisthesis is usually caused by degenerative disk disease and often affects women over 40 years of age. If too much slippage occurs, the bones may begin to press on nerves and surgery may be necessary to correct the condition.

Causes Genetics: There may be a hereditary aspect to spondylolysis. An individual may be born with thin vertebral bone and therefore be vulnerable to this condition. Significant periods of rapid growth may encourage slippage.

Overuse: Some sports, such as gymnastics, weight lifting and football, put a great deal of stress on the bones in the lower back. They also require that the athlete constantly over-stretch (hyperextend) the spine. In either case, the result is a stress fracture on one or both sides of the vertebra.

Spondylolisthesis may also develop because of degenerative changes in the vertebral joints and certain medical conditions such as cerebral palsy.

Symptoms - In many people, spondylolysis and spondylolisthesis are present, but without any obvious symptoms. Pain usually spreads across the lower back, and may feel like a muscle strain.

Spondylolisthesis can cause spasms that stiffen the back and tighten the hamstring muscles, resulting in changes to posture and gait. If the slippage is significant, it may begin to compress the nerves and narrow the spinal canal.

Diagnostic tests - X-rays of the lower back (lumbar) spine will show the position of the vertebra. Usually, spondylolisthesis occurs in the last lumbar vertebra, just above the tailbone (sacrum).

If the vertebra is pressing on nerves, a CT scan or MRI may be needed before treatment begins to rule out any other contributing conditions.

Treatment - Initial treatment for spondylolysis is always conservative. The athlete should take a break from the activities until symptoms go away, as they often do. Anti-inflammatory medications such as ibuprofen may help reduce back pain. Occasionally, a back brace and physical therapy may be recommended. Epidural steroid injections may also help alleviate inflammation and ease pain. In most cases, activities can be resumed gradually and there will be few complications or recurrence. Stretching and strengthening exercises for the back and abdominal muscles can help prevent future stress fractures.

Periodic X-rays will show whether the bone is continuing to slip. Surgery may be need if slippage continues, or if the back pain does not respond to conservative treatment and begins to interfere with activities of daily living. This is more often the case with degenerative spondylolisthesis.

Usually, two procedures are performed, one to relieve the nerve compression and the second to ensure spinal stability. The first procedure, called a decompressive laminectomy, removes part of the bone that is pressing on the nerves. This reduces irritation and inflammation, but increases the instability of the spine. Hence the need for the second procedure, called spinal fusion.

In spinal fusion, a piece of bone is transplanted to the back of the spine. As the bone heals, it fuses with the spine and helps to stabilize it. Sometimes, an internal brace of screws and rods is used to hold the vertebra together as the fusion heals.

Spinal Stenosis Back aches and pains are a health concern for millions of people. Nearly 12 million Americans annually see their doctors because of back aches and pains. There may be many reasons for backaches and pains. One cause could be spinal stenosis. Stenosis means narrowing. In spinal stenosis, the spinal canal, which contains and protects the spinal cord and nerve roots, narrows and pinches the spinal cord and nerves. The result is low back pain as well as pain in the legs. Stenosis may pinch the nerves that control muscle power and sensation in the legs.

Causes of spinal stenosis - There are many potential causes for spinal stenosis, including: Aging. As you get older, the ligaments (tough connective tissues between the bones in the spine) can thicken. Spurs (small growths) may develop on the bones and into the spinal canal. The cushioning disks between the vertebrae may begin to deteriorate. The facet joints (flat surfaces on each vertebra that form the spinal column) also may begin to break down.

Heredity. If the spinal canal is too small at birth, symptoms may show up in a relatively young person.

Changes in blood flow to the lumbar spine.

Symptoms of spinal stenosis

Pain and difficulty when walking, aggravated by activity.

Numbness, tingling, hot or cold feelings, weakness or a heavy and tired feeling in the legs.

Clumsiness, frequent falling, or a foot-slapping gait.

Diagnosing spinal stenosis These symptoms also can be caused by many other conditions, which makes spinal stenosis difficult to diagnose. There is usually no history of back problems or any recent injury. Often, unusual leg symptoms are a clue to the presence of spinal stenosis.

If simple treatments, such as postural changes or nonsteroidal anti-inflammatory drugs, do not relieve the problem, your orthopaedic surgeon may request special imaging studies to determine the cause of the problem. An MRI (magnetic resonance image) or CAT (computed tomography) scan may be requested. A myelogram (an X-ray taken after a special fluid is injected into the spine) may be arranged. These and other imaging studies provide details about the bones and tissues and assist the orthopaedic evaluation.

Treatment - Conservative treatment Changes in posture. People with spinal stenosis may find that flexing the spine by leaning forward while walking relieves their symptoms. Lying with the knees drawn up to the chest also can offer some relief. These positions enlarge the space available to the nerves and may make it easier for stenosis sufferers to walk longer distances.

Medications. Sometimes the pressure on the nerves is caused by inflammatory swelling. Nonsteroidal anti-inflammatory medication such as aspirin or ibuprofen may help relieve symptoms.

Rest, followed by a gradual resumption of activity, also can help. Aerobic activity such as bicycling is often recommended.

Losing weight can also relieve some of the load on the spine.

When stenosis causes severe nerve root compression, these treatments may not be enough. Back and leg pain may return again and again. Because many stenosis sufferers are unable to walk even short distances, they often confine their activities to the home.

Surgical treatment - If conservative treatment does not relieve the pain, your orthopaedic surgeon may recommend surgery to relieve the pressure on affected nerves. In properly selected cases, the results are quite satisfactory, and patients are able to resume a normal lifestyle. Jun 2001

Low Back Pain - Why is low back pain common? Low back pain is one of the most frequent problems treated by orthopaedic surgeons. Four out of five adults will experience significant low back pain sometime during their life. After the common cold, problems caused by the lower back are the most frequent cause of lost work days in adults under the age of 45.

The lower or lumbar spine is a complex structure that connects your upper body (including your chest and arms) to your lower body (including your pelvis and legs). This important part of your spine provides you with both mobility and strength. The mobility allows movements such as turning, twisting or bending; and the strength allows you to stand, walk and lift. Proper functioning of your lower back is needed for almost all activities of daily living. Pain in the lower back can restrict your activity and reduce your work capacity and quality of enjoyment of everyday living.

How is low back pain diagnosed? Most cases of low back pain are not serious and respond to simple treatments. Your orthopaedist can accurately diagnose and effectively treat most types of low back pain in the office. You will be asked about the nature of your symptoms and whether you sustained an injury. You also will have an examination of your spine and legs. For many episodes of low back pain no expensive tests are needed for initial assessment and treatment.

If your pain is severe and not responding to treatment or if you have significant leg pain, some imaging tests may be required. Plain X-rays will show arthritis and bone diseases, but will not show soft tissues such as the lumbar disks or nerves. For conditions or injuries that involve these soft tissues, CT scan (computerized tomography) or MRI (magnetic resonance imaging) may be needed. Occasionally, a bone scan will be needed to assess bone activity and electrical tests, EMG (electromyography) may be needed to determine if the spine condition has caused nerve or muscle damage.

What are the common causes? Low back pain can be caused by a number of factors from injuries to the effects of aging.

Low Back Sprain and Strain - The muscles of the low back provide power and strength for activities such as standing, walking and lifting. A strain of the muscle can occur when the muscle is poorly conditioned or overworked. The ligaments of the low back act to interconnect the five vertebral bones and provide support or stability for the low back. A sprain of the low back can occur when a sudden, forceful movement injures a ligament which has become stiff or weak through poor conditioning or overuse.

These injuries, or sprain and strain, are the most common causes of low back pain. Frequently, a combination of other factors may increase the likelihood of injury orddisease:

poor conditioning improper use obesity smoking

The natural effects of normal aging on the body, in general, and low back, in particular, are osteoporosis or decreased amount of bone; decrease in strength and elasticity of muscles; and decrease in elasticity and strength of ligaments. Although you cannot totally halt the progress of these effects, they can be slowed by regular exercise, knowing the proper way to lift and move objects, proper nutrition, and avoidance of smoking.

Age - "Wear and tear" and inherited factors will cause degenerative changes in the disks, called degenerative disk disease, and arthritic changes in the small joints. These changes occur to some degree in everyone. When severe, they can cause low back stiffness and pain. Arthritic bone spurs and inflamed joints can cause nerve irritation and leg pain. Almost everyone develops "wear and tear" changes in their low back as they age, although for most people it causes little pain or loss of function.

Osteoporosis and Fractures - All bones lose bone strength over time and the lumbar vertebrae, particularly in postmenopausal women, can be fractured or compressed from a fall or even from the stress of lifting or everyday activities.

Protruding Disk - The disk is composed of a soft center or nucleus, which, in children and young adults, is jelly-like. The nucleus is surrounded by a tougher outer portion called the anulus. With normal aging, the nucleus begins to resemble the anulus. During middle-age, fissures or cracks may occur in the disk. These may be the source of back pain. If the crack extends out of the disk, material from the disk may push out or rupture. This often is referred to as a herniated or slipped disk. If the protruded disk presses a nerve, it may cause pain in the leg.

What is the best treatment? Most low back pain can be safely and effectively treated following an examination by your orthopaedic surgeon and a prescribed period of activity modification and some medication to relieve the pain and diminish the inflammation. Although a brief period of rest may be helpful, most studies show that light activity speeds healing and recovery. It may not be necessary for you to discontinue all activities, including work. Instead, you may adjust your activity under your orthopaedist's guidance.

Once the initial pain has eased, a rehabilitation program may be suggested to increase your muscle strength in your low back and abdominal muscles as well as some stretching exercises to increase your flexibility. Weight loss if you are overweight, and quitting smoking if you are a smoker, also will decrease the chances of a recurrence of your low back pain. The best long-term treatment is an active prevention program of maintaining your physical condition and observing proper lifting and postural activities to prevent further injuries.

When is surgery needed? Most low back pain, whether acute or chronic, almost always can be treated without surgery. The most common reason for surgery on the lower back is to remove the pressure from a "slipped disk" when it causes nerve and leg pain and has not responded to other treatments. Some arthritic conditions of the spine, when severe, also can cause pressure and nerve irritation, and often can be improved with surgical treatment.

What is the lower back? Your lower back is a complex structure of vertebrae, disks, spinal cord, and nerves. There are:

five bones called lumbarvvertebrae - stacked one upon the other, connecting the upper spine to the pelvis

six shock absorbers called disks - acting both as cushion and stabilizer to protect the lumbar vertebrae

spinal cord and nerves - the "electric cables" which travel through a central canal in the lumbar vertebrae, connecting your brain to the muscles of your legs

small joints - allowing functional movement and providing stability

muscles and ligaments - providing strength and power and at the same time support and stability

Prevention The normal effects of aging that result in decreased bone mass, and decreased strength and elasticity of muscles and ligaments, can't be avoided. However, the effects can be slowed by:

exercising regularly to keep the muscles that support your back strong and flexible

using the correct lifting and moving techniques; get help if an object is too heavy or an awkward size

maintaining your proper body weight; being overweight puts a strain on your back muscles

avoid smoking

maintaining a proper posture when standing and sitting; don't slouch

Your orthopaedist is a medical doctor with extensive training in the diagnosis and nonsurgical and surgical treatment of the musculoskeletal system, including bones, joints, ligaments, tendons, muscles and nerves.

This brochure has been prepared by the American Academy of Orthopaedic Surgeons and is intended to contain current information on the subject from recognized authorities. However, it does not represent official policy of the Academy and its text should not be construed as excluding other acceptable viewpoints.

\3 gangrene poisoning

(Gas Gangrene, Food Poisoning) What is it? Organism causes gas gangrene food poisoning

Bacteria: gram-pos spore forming Spores found in soil and food

Who gets it? People who get spores into open trauma wounds, where the bacteria can then grow. Food poisoning: people who eat food contaminated with spores

How is it spread? Not commonly transmitted from person to person. most often assoc with war wounds, car accidents, complicated abortions.

Food poisoning: not commonly transmitted from person to person. The spores survive cooking, and grow especially in reheated foods (eg, meat dishes). The eaten bacteria then produce a toxin which causes diarrhea

What are the symptoms of the infection? Pain and swelling with presence of gas in affected tissue. Jaundice, and bloody pus may be seen. Shock and death may occur.

Food poisoning: About half a day after eating organisms, patients get a watery diarrhea with cramps

Diagnosis - organisms can be found in tissue samples from wounds. Food poisoning: organisms can best be found in uneaten food

Treatment - Antibiotics (penicillin), and dead tissue should be cut out of the wound. Food poisoning: no antibiotics necessary. Typically diarrhea ends after 24 hours.

Prevention - wounds should be cleaned (dead tissue removed immediately) and penicillin could be given to prevent gas gangrene.

Food poisoning: nothing specific can be done. Cook food long enough to kill the bacteria

Gangrene is defined as the destruction of living tissue due to obstruction of the blood and oxygen supply. The bacteria which causes the infection is known as Clostridium (gas gangrene) or a combination of streptococci and staphylococci (Meleney's synergistic gangrene).

Gangrene occurs when the blood supply to part of the body is cut off. This depletes the tissues of oxygen and they begin to die. Gangrene usually affects the extremities, such as the toes, feet, legs, fingers, hands, and arms. It may also occur in other parts of the body, including the abdomen or intestines. Gangrene usually occurs after trauma or surgery. Usually gangrene begins 24 hours to 3 days after trauma but may occur anywhere from 3 hours to 6 weeks later. As the tissue begins to die, carbon monoxide and hydrogen gases are released, causing bubbling around the tissue.

There are two (or three) types of gangrene:  dry gangrene, a condition in which the tissues dry and slough off because the blood vessels are no longer supplying blood to the area  wet or gas gangrene, which is usually caused from a bacterial infection of a wound

DRY GANGRENE - Dry gangrene is caused by the gardual loss of blood. Dry gangrne often comes about as a result of diabetes, arteriosclerosis, or severe frostbite. The skin becomes painful and them becomes dark, and then the dead skin eventually dries and drops off. This form of gangrene is not life threatening because healing usually takes place naturally at the junction between the living and dead tissue.

MOIST GANGRENE - A more serious condition, known as moist gangrene, is caused by the loss of blood supply. Some cells may stay alive while surrounding cells begin to quickly die and begin to leak fluid, which causes the affected tissues to become moist. Because of the moist environment, bacteria begin to fluorish. When moist gangrene first has its affects the skin becomes swollen and blisterous, and then becomes foul smelling. This type of gangrene can spread rather quickly and can be fatal.

Gas Gangrene (clostridial myositis and myonecrosis) - The most deadly form of gangrene is known as gas gangrene. It occurs in wounds which are affected by bacteria that live in low oxygen environments, which release gas and poisons into the body. The symptoms of gas gangrene are high fever, brown pus, and gas bubbles on the skin. This form of gangrene spreads eery quickly, and causes a rapid death. The preferred treatment is a combination of hyperbaric oxygen (HBO,), surgery, and antibiotics.

Gas gangrene is an acute, rapidly progressive, non-pyogenic, invasive clostridial infection of the muscles, characterized by profound toxemia, extensive edema, massive death of tissue, and a variable degree of gas production.

Gas gangrene is either an endogenous infection, caused by contamination from a clostridial focus in the body, or an exogenous infection, mostly in patients with compound and/or complicated fractures with extensive soft tissue injuries after street accidents.

The infection is caused by anaerobic, spore-forming, Grarnpositive encapsulated bacilli of the genus clostridium. More than 150 species of clostridium have been recognized but the most commonly isolated is C. perfringens (95 %) either alone or in combination with other pathogenic clostridia,

For the induction of gas gangrene, two conditions have to be fulfilled: the presence of clostridial spores and an area of lowered oxidation-reduction potential caused by circulatory failure in a local area or by extensive soft tissue damage and necrotic muscle tissue. This condition results in an area with a low oxygen tension where clostridial spores can develop into the vegetative form.

The onset of gas gangrene may occur between 1 and 6 hours after injury and presents with severe and sudden pain in the infected area. The skin overlying the wound in the early phases appears shiny and tense and then becomes dusky and progresses to a bronze discoloration. The infection can advance at a rate of 6 inches per hour. Any delay in recognition or treatment may be fatal. Hemorrhagic bullae or vesicles may also be noted. A thin, sero-sanguinolent exudate with a sickly, sweet odor is present. Swelling and edema of the infected area is pronounced. The muscles appear dark red to black or greenish, are noncontractile, and do not bleed when cut.

Mortality in the series of Him (34) was 28%. He concluded that mortality and morbidity could be reduced if the disease is recognized early and appropriate therapy applied promptly. He recommends adequate and operative debridement, antibiotics, HBO,, and surgical intensive care.

Symptoms of gangrene may include:  a crackling or rubbing sensation under the skin  severe pain and swelling at the site of injury  numbness at the site of the infection  discoloration of the skin, often starting as white and eventually becoming brownish-reddish or black color  dark and red or black muscles and bones if the skin breaks open  frothy, watery, foul smelling discharge  fever, with a temperature around 101 degrees F  pale skin  decreased activity  rapid heart beat

Causes and risks of the infection include:  a blockage of blood to an organ or tissue  surgery causing tissue damage  trauma or injury, such as frostbite, boils, crush injuries, and severe burns, that destroys tissues in the body  infection of wounds, especially deep wounds  certain diseases that affect circulation, including atherosclerosis, diabetes, and Raynaud's disease  blood clots, such as a deep venous thrombosis  a ruptured appendix caused by appendicitis  an intestinal hernia  smoking and drinking alcohol

-PREVENTION - The best way to prevent the cause of gangrene is to keep any skin injury clean and watch for redness, discoloration, and or puffiness. A person may be able to prevent gangrene in some instances by:  following sports safety guidelines for children, adolescents, and adults  getting prompt treatment for deep wounds, burns, crush injuries, or frostbite  getting treatment for diabetes, Raynaud's disease, and atherosclerosis  avoiding cigarettes and alcohol

The tests for gangrene are: gram stain of fluid from infected areas anaerobic tissue and fluid culture shows Clostridium X-Ray, CT scan, or MRI shows gas gangrene.

Long term effects of gangrene may include: permanent death of the tissues in the area affected, amputation of the affected limb or removal of the affected organ. sepsis, or blood poisoning, shock, death, especially with gangrene of the abdomen or the bowels, if gangrene goes untreated. Gangrene poses no risk to others.

The best way to treat gangrene is to remove the dead and infected tissue surgically. Amputation may be neccessary. Antiobiotics are also given (such as penicillin)


\4 migraine headaches

When should you be worried? Sometimes when we are in the midst of a gripping headache and medication does not help, we may wonder if this headache is a sign or symptom of something sinister occurring in the brain. When should we be concerned about headaches? When do we need expert advice from specialists? You should seek expert advice from a neurologist or neurosurgeon for your headache if you answer yes to any of the questions below: Is this the first or worst headache that you have ever experienced? Is there associated nausea, vomiting or fever? Are there mental changes such as confusion, delirium or fainting episodes? Are you taking any new medications? Are the headaches daily?

Diagnosis of Headaches If the signs and symptoms of your headache are similar to the ones described earlier, you are advised to consult a neurologist or neurosurgeon. A detailed history and complete neurological examination is required, following which your neurologist or neurosurgeon may order a brain scan. This may be either a CT (Computerised Tomographic) scan or an MRI (Magnetic Resonance Imaging) scan. If there is an abnormality, then the various treatment options will be discussed with you. The neurologists and neurosurgeons at the Brain Centre, Singapore General Hospital are equipped with the most modern and sophisticated tools to comprehensively assess your condition.

In general, headaches that require specialist attention can be broadly categorised into two groups: Headaches due to disease (pathology) Chronic recurring headaches; see below

Headaches Due to Disease (Pathology) - There are 3 main groups of conditions which can give rise to these headaches.

A. Brain Pathology Stroke - These headaches are usually described as sudden, very severe, and associated with drowsiness and weakness of the limbs. Acute brain haemorrhage such as subarachnoid haemorrhage from a ruptured aneurysm (dilation of a blood vessel, usually an artery, producing a pulsating swelling) is a neurosurgical emergency and demands urgent medical attention. Similarly, haemorrhages from uncontrolled hypertension need neurosurgical care. Brain tumours - There are a wide range of brain tumours, some of which are malignant and others which are benign that could cause headaches. These headaches are usually described as progressive, worse in the mornings, associated with nausea and vomiting, sometimes one-sided, and sometimes causing neurologic deficits such as weakness of the limbs, facial numbness or double vision. These tumours can also affect the circulation of cerebrospinal fluid and result in a condition called hydrocephalus in which the brain becomes swollen. Inflammation - Usually this is associated with infection, such as meningitis. There is fever, neck stiffness and drowsiness apart from the headaches.

B. Local Pathology The areas of the head and neck are also vulnerable to diseases which can result in headaches. For example, sinusitis, eye and ear infection or inflammation of the temporal artery can all result in bad headaches. These headaches may be associated with nasal congestion, eye swelling, earache, or even mouth or jaw pain.

C. Systemic Pathology Similarly, systemic diseases such as uncontrolled hypertension can result in headaches. These headaches tend to be more non-specific and are usually relieved with the appropriate analgesics. Sometimes they are caused by new medications for chronic medical conditions which are not tolerated by the individual.

Chronic Recurring Headaches - There are mainly 2 types of chronic recurring headaches.

A. Vascular (Migraine) Type Headaches These migraine attacks occur in individuals who are predisposed to this condition and may be precipitated by factors such as bright lights, stress, diet changes and trauma. Common migraine headaches are usually episodic and associated with photophobia. Sometimes there are neurologic deficits (such as weakness of the limbs, facial numbness or double vision) but these usually resolve within 24 hours. There is a spectrum of treatment options available for migraine type headaches, and your neurologist is the best person to decide the best medication for you .

B. Muscle Contraction (Tension) Type Headaches These headaches are caused by fatigue, worry, stress or poor posture. Usually explanations and reassurance are the mainstay of treatment, but there are medications which can be prescribed if necessary.

All of us suffer from an occasional headache; in fact, 20 million Americans see their doctors each year because of headaches. Although headaches can be very uncomfortable and temporarily disabling, most are not associated with serious illness and can be relieved by resting in a quiet room or by taking a nonprescription painkiller, such as aspirin or acetaminophen. Some types of headaches, however, may require stronger prescription medications, and others are warning signs to seek immediate medical attention.

These warning signs include: Severe, sudden headaches that seem to come on like a "bolt out of the blue."

Headaches accompanied by loss of consciousness, alertness or sensation; confusion, visual blurring, or other neurological changes.

Recurrent headaches affecting one particular area, such as an eye, temple, etc.

Recurrent headaches of increasing intensity or frequency. Headaches accompanied by neck stiffness and fever.

Any unexplained change in the nature or frequency of headaches. Headaches that wake you up.

TENSION HEADACHES - The most common headaches are those associated with tension or muscle contractions and are directly related to stress. The pain tends to be steady and dull rather than throbbing. It is usually felt in the temples, forehead, neck, or back of the head. Sometimes, the pain seems to encircle the head like a tight band. Tension headaches may occur at any time, but are most commonly experienced during periods of stress or worry.

Treatment involves relieving the tension through massage, heat, a hot shower, relaxation techniques or any activity that puts aside the worries of the moment. Nonprescription painkillers, such as aspirin or acetaminophen, may also help. For severe muscle tension headaches, other slightly more potent drugs may be prescribed. These drugs may cause drowsiness and slow reflexes and should be taken with caution by people who work with machinery or drive. Most doctors also recommend that such medication be used for only short periods of time (not more than a few days).

MIGRAINE HEADACHES - Migraine headaches vary from person to person, but typically they are throbbing headaches affecting one side of the head. They are often accompanied by a number of other symptoms, which also vary according to individual cases. Some people have very little head pain but suffer from distorted vision and hearing or feelings of intense anxiety. Others may suffer from incapacitating pain lasting for several days. Most migraine patients fall between these two extremes.

Many people are warned of an impending migraine attack by bizarre distortions of size, position, time and place  the so-called "Alice-in-Wonderland syndrome." Others see flashing lights or bright colors in unusual shapes. Nausea, vomiting, chills, fever, dizziness, diarrhea; abdominal, arm, or leg pain; and sensitivity to light are still other symptoms that may accompany a migraine.

Regardless of the differing symptoms, all migraine headaches are related to changes in the blood vessels of the head and neck. This is why they are often referred to as vascular headaches. Early warning symptoms of a migraine are thought to be caused by a narrowing of these blood vessels, while the head pain is believed to be a result of the subsequent expanding or dilating of the vessels. What causes these changes is unknown, although many researchers now believe that chemicals produced in the body that act on the blood vessels may be responsible. The drawing at the top shows the blood supply to the brain. Changes in the size of any of these blood vessels can lead to vascular headaches. The drawing at the bottom shows the scalp and facial muscles that can cause tension headaches.

TRIGGERING FACTORS - Dozens of factors appear to trigger a migraine in susceptible individuals; again, these vary from person to person. Common precipitating factors include hormonal changes, particularly those associated with menstruation or use of birth control pills; sudden changes in the weather or temperature, emotional factors, certain foods or additives, especially the preservatives in cured meats, monosodium glutamate (MSG), or caffeine, chocolate, cheese, and corn products; drugs; glaring lights; strong odors, and cigarette smoke. Avoiding these triggering factors can solve the problem for many people. Others, however, may require further treatment.

TREATING MIGRAINE - Unfortunately, there is no cure for migraine headaches, although most can be controlled through avoiding triggering factors and by drugs and other therapies. Over-the-counter analgesics may help some migraine patients, especially children, but most adult sufferers require additional or alternative medications. The most successful treatments are those that either prevent an attack or stop it in its earliest stages. Ergotamine or drugs related to ergot derivatives may be prescribed to be taken at the first warning signs of a migraine. These drugs constrict or narrow the arteries, thus relieving the pain from the expanded cranial vessels. They should not be taken by people who have hardening of the arteries, high blood pressure, angina, coronary disease or other circulatory problems; severe infections, or disorders of the kidney or liver. And since they narrow the blood vessels, these medications should be used with caution by anyone who will be exposed to the cold, which further reduces blood flow to the arms and legs.

Another treatment involves taking a beta-blocking drug, which prevents the expanding of the cerebral arteries and thus prevents migraine attacks. Since these drugs slow the rate of heartbeats, they are often contraindicated for heart patients. They also should not be used by people with asthma or diabetes.

Only a doctor can determine whether a particular prescription drug is indicated for individual migraine cases. If a prescription is given, it is important to use the drug only as directed.

CLUSTER HEADACHES - Cluster headaches are a rare variant of migraine, which strike several times in rapid succession. They are most often experienced by men and are extremely painful. The drugs used to treat a migraine are often prescribed for administration early in an attack. Therefore, they are often administered by injection or suppository to allow the medication to enter the bloodstream rapidly.

SINUS HEADACHE - Sinus headaches are associated with a swelling of the membranes lining the sinuses (spaces) of the nasal passages. The pain tends to be dull and may shift if the head is moved in a certain way. Sinus headaches may be relieved by simple painkillers or, in some cases, a decongestant to relieve the swelling.

SUMMING UP - The vast majority of headaches are not medically serious. Most can be controlled by the use of simple medications and by altering habits or lifestyle, as in the case of frequent tension headaches.

If you are concerned about and difference in your treatment plan and the info in this article, you are advised to contact your health care provider.

What causes headaches? Despite the pain you're feeling and the place it seems to originate, it's not your brain that's aching; it has no pain receptors. It's the skin, muscles, and blood vessels that cover the skull and the nerves that run from your brain to your head and face that cause the discomfort we call a headache. Different types include tension headaches, migraines, and cluster headaches. High blood pressure, eye or sinus problems, and brain tumors or infections can also cause head pain in rare cases.

How do I know which type I have? Each of the three major headache types has different symptoms and responds to different treatments. Here's what you need to know about each:

Tension headaches

Why you hurt

Pain results from stress-related muscle tension in the neck, shoulders, and head. Researchers think that fluctuations in brain chemicals called neurotransmitters, which regulate the perception of pain, may also play a role.

Symptoms

 a dull ache frequently described as a viselike squeezing of the head, sometimes accompanied by a stiff or sore neck

 pain usually above the eyes or in the back of the head

 usually moderate pain

 pain may fade in and out over the course of a day or several days

What to do - For occasional tension headaches, try over-the counter analgesics: aspirin, acetaminophen, or ibuprofen. But be careful not to overuse them; that can lead to so-called rebound headaches (headaches brought on by withdrawal from these medications). For chronic headaches, see your doctor; prescription migraine drugs or antidepressants (which can also block pain signals) can often help if your headaches are unusually severe or frequent. To prevent tension headaches, stay away from activities that strain your neck muscles, such as reading while looking down. Consider acupuncture too; many tension headache sufferers say regular treatments lessen both the severity and frequency of their headaches.

Migraines - Why you hurt - During a migraine the blood vessels in your head swell and press on nearby pain receptors. Fluctuations in levels of neurotransmitters may also play a role. Other possible triggers include hormonal changes that accompany menstrual periods (most migraine sufferers are women), oral contraceptives, changes in sleep patterns, skipping meals, changes in weather, bright or flashing lights, excessive noise, stress, and some foods -- particularly chocolate, red wine, aged cheeses, and smoked meats. Your genes may also predispose you to getting migraines. Most people who get migraines have their first attack before age 30.

Symptoms  mild to severe pulsing or throbbing pain, usually on one side of the head, that lasts from several hours to several days

 pain usually gets worse if you move around or look at bright light or hear loud noise

 pain often interferes with daily activities and may cause nausea or vomiting

 headaches are sometimes preceded by visual changes called auras that are probably caused by the blood vessels constricting before they swell and thus reducing blood flow to the brain. During an aura you may lose your vision or see shimmering, jagged, or flashing lights or colors. Some people also feel nauseated or irritable right before a migraine begins.

What to do - Over-the-counter pain relievers such as aspirin and other analgesics can be helpful for mild cases. But for frequent or severe migraines, prescription drugs are probably your best bet. Your doctor can help you choose from a wide range, including beta blockers and calcium channel blockers, which keep blood vessels from swelling, and antidepressants, which increase neurotransmitter levels. Acupuncture, relaxation exercises, yoga, biofeedback, and the herbal remedy feverfew can also be helpful. Of course you should also eat regular meals, get plenty of sleep, and avoid foods that trigger migraines for you. Drugs like ergotamine and sumatriptan can help stop a migraine once it starts.

Cluster headaches Why you hurt - Cluster headaches are much less common than tension headaches or migraines. Like migraines, they are caused by swelling blood vessels in the head. Some researchers suspect that people get cluster headaches when they are not getting enough oxygen for some reason. Fluctuating neurotransmitter levels may play a role. Other suspected triggers include alcohol, cold or hot wind, high altitude, stress, and smoking. Cluster headaches occur most often in spring or fall. Most sufferers are male.

Symptoms  knifelike pain limited to one side of the head, often in or around one eye, that usually lasts no more than an hour

 headaches in clusters, either several times in one day or for several days in a row, with recurrences at the same time of day, usually for six to eight weeks at a time

 nighttime onset, perhaps painful enough to wake you

 tearing in the eye on the affected side, or redness or swelling around the eye, or a droopy eyelid

 a stuffy or runny nose along with the headache

What to do To prevent cluster headaches from occuring, doctors usually prescribe migraine medications. Once you have pain, inhaling oxygen is the only treatment known to bring relief. Herbal remedies also show promise. Feverfew may ease the pain of cluster headaches, but can have side effects like mouth ulcers.

When should I see a doctor about a headache?  your headaches get stronger and more frequent

 your headaches last more than 24 hours or recur two or three times per week

 if you also have numbness, blurred vision, memory loss, or dizziness

 if you get a headache after hitting your head

 if exercise brings on the headache

 if your headaches interfere with daily life

 if your headache is accompanied by a fever over 100 degrees, you find it painful to bend your head forward, or light hurts your eyes

 if the headache is accompanied by nausea, vomiting, or drowsiness

 if you have severe pain around one eye with blurred vision

Cough Headache - The term cough headache refers to headaches triggered immediately by coughing. These same headaches can also be induced by sneezing, laughing, straining at stool, lifting a heavy object, and bending the head down towards the ground. They come in two varieties: the benign, which are unassociated with any discernable neurologic disease, and the symptomatic, which are due to impaction of herniated cerebellar tonsils at the foramen magnum. These latter are almost always due to a congenital abnormality (called a Chiari I malformation) in which the cerebellar tonsils project through the foramen magnum into the region of the upper cervical spinal cord, but rarely a tumor may herniate the tonsils through the foramen magnum. Both the benign and symptomatic types are rare; The symptomatic may be the slightly more common of the two. These headaches have now been clearly distinguished from exertional and sexual headaches to which they were linked in the past.

Benign cough headache - features Onset: Abrupt Duration: Seconds to minutes generally Intensity: Moderate to severe Quality: Sharp or splitting Location: Bi-occipital generally, not invariably

Accompaniments - None--no nausea or vomiting

Age of onset - 40 to 80 years roughly (mean age late 60s)

Genders affected - Strong male predominance: 80% are males

Symptomatic cough headache - features Onset: Abrupt Duration: Seconds to minutes generally Intensity: Moderate to severe Quality: Sharp or splitting Location: Bi-occipital generally, not invariably

Accompaniments - May be none initially, but posterior-fossa symptoms, such as faintness, numbness of face or limbs, and difficulty in swallowing, develop in most

Age of onset - 15 to 60 years roughly (mean age late 30s)

Genders affected - Roughly equal prevalence in both genders

Differentiating benign from symptomatic cough headache - The benign and the symptomatic types can not be differentiated by the features of the headaches. However, the presence of accompanying symptoms of posterior fossa involvement (see section just above) indicate that the headaches are symptomatic of hindbrain herniation. Also indicative of herniation are headaches beginning under the age of 40 and headaches unresponsive to indomethacin (see below). On the other hand, headaches beginning in a man over the age of 50 and headaches eliminated by treatment with indomethacin are most likely benign. Experts recommend that a magnetic resonance image (MRI) of the brain with good sagittal views of the foramen magnum be obtained in all patients with cough headaches.

However, patients over 50 years of age without posterior fossa signs and with a good response to indomethacin can be followed safely without MRI images as long as their course is stable. The demonstration by the MRI images that the tips of the cerebellar tonsils are more than 3 mm caudal to the rim of the foramen magnum (a Chiari type I malformation or hindbrain herniation) does not by itself prove that headaches are symptomatic, for many such abnormalities are not symptomatic, because they do not occlude the free flow of spinal fluid in the subarachnoid space. However, the absence of any abnormality clearly shows that the headaches are not symptomatic.

Diagnostic criteria of the International Headache Society for benign cough headache From the above presentation of contemporary information on the cough headaches, one can see that the diagnostic criteria of the IHS published in 1988 need revision. Its criteria are as follows:

Is a bilateral headache of sudden onset, lasting less than one minute, precipitated by coughing. May be prevented by avoiding coughing May be diagnosed only after structural lesions such as posterior fossa tumour have been excluded by neuroimaging.

Treatment of benign cough headache Indomethacin capsules (by prescription) are very effective in the prevention of these cough headaches in almost all patients. I generally begin with one 25 mg capsule three times daily. After a good response is obtained, smaller doses should be tried. Some patients may need up to 2 capsules thrice daily for adequate prevention. When this drug is ineffective or contraindicated at any time during therapy, then performing a therapeutic lumbar puncture should be considered, for Raskin (1995) has reported that nearly half of the patients in his small series had prolonged relief from cough headaches after one or two LPs in which 40 ml of spinal fluid were removed.

Alleviative medications are worthless once a cough headache has been triggered, since the headache would be gone before the medication is absorbed into the body.

Treatment of symptomatic cough headache Neither indomethacin nor other drugs are known to prevent symptomatic cough headaches. Their only therapy is suboccipital craniectomy (surgical decompression of the foramen magnum), which prevents the low-lying cerebellar tonsils from obstructing the flow of spinal fluid from the cerebral to the spinal subarachnoid space.

Example of a man with benign cough headache This 66-year-old man told me, in May 1997, that his headaches began in September 1996. He said that when he coughs or sneezes he immediately experiences a severe pain in his head. This same headache is also triggered by bending his head and body towards the ground, as in tying his shoelaces while seated in a chair. Tightening his lower back or abdominal muscles, as in lifting a heavy object or straining at stool, also triggers a headache. When he puts his foot on a chair to tie his shoelaces a headache does not appear, nor does one appear when he bends his knees to a full squat to pick up an object from the floor. When the pain is triggered by bending over, it disappears within 1/2 to 2 minutes after he straightens up. The duration of his cough-induced headaches is similar. Soon after getting out of bed in the morning, he can bend over to tie his shoelaces without triggering a headache. Headaches occur every day, but only after the above actions. Repetitive physical activities, such as cutting wood, do not trigger headaches.

Most of his headaches strike the left temple, but others occur in the right temple or across the back of the head. The pain feels like he has been hit in the head by a baseball bat, or like an intensly tight band on his head. It is similar to the pain he has experienced from eating a big scoop of ice cream.

He had a normal MRI and physical and neurologic examinations. I recommended that he take 25 mg indomethacin capsules, beginning with one three times daily. He did so, and his headaches ceased to occur. He then decreased his dose to one capsule twice daily without return of headaches. When I last heard from him, in September 1997, he said he was decreasing the dose to one capsule daily.

Example of a woman with symptomatic cough headache This example is abbreviated from Case 1 in an article by Nightingale and Williams (1987). This 28-year-old woman had headaches for 15 months provoked by coughing, laughing, and straining at stool. Headaches began within seconds of the precipitant, worsened for a few seconds, and then faded away. Between attacks, she was well, and she had neither neurological symptoms nor signs. The cerebellar tonsils were shown to be descended through and obstructing the foramen magnum. After the foramen was surgically decompressed, she was free from headaches and remained so for a 10-year follow up.

- Diag and Treatment of Headache Emergencies -

New-severe or worst-ever headache of abrupt onset (thunderclap type) Causes - Subarachnoid hemorrhage, "crash" migraine, unclassifiable headaches, venous-sinus thrombosis, unruptured arterial aneurysm at the circle of Willis, dissection of a carotid or vertebral artery, and benign exertional or coital headache.

Incidences - In a study by Harling et al. (1989), 71% of 49 patients admitted for instantaneous severe generalized headache had CT or CSF proof of subarachnoid hemorhage. Among these, 77% had a ruptured aneurysm, 6% bled from an arterio-venous malformation (AVM), and 17% had normal 4-vessel angiograms (unknown source of hemorrhage).

Long follow up (mean 3.3 years) by Wijdicks et al. (1988) of 71 patients initially suspected to have subarachnoid hemorrhage, but with normal CT and CSF findings, showed a benign course in all. Hence, the incidence of cerebral venous-sinus thrombosis (Bruijn de SFTM, et al., 1996), unruptured aneurysm, and dissection of a carotid or vertebral artery as a cause of thunderclap headache must be relatively low. Nevertheless, unruptured aneurysms can cause thunderclap headache as initially reported by Day and Raskin (1986). Confirmation comes from a study of unruptured aneurysms by Raps et al. (1993).

Comments on features of thunderclap headaches from structural causes The abrupt pain of subarachnoid hemorrhage may begin unilaterally, but soon becomes bilateral, generally with strong involvement of the posterior head and neck. Neck stiffness is not an invariable examination finding, though it is found in the majority of cases. In most instances, one can not reliably distinguish the thunderclap headache of subarachnoid hemorrhage from the other causes. The pain from an unruptured cerebral aneurysm is sometimes accompanied by an oculomotor palsy. This pain is probably either from aneurysmal expansion or thrombosis, or bleeding into the wall of the vessel. The pain of a dissection of the carotid artery, may be localized to the head (the frontal region), and is generally accompanied by a Horner's syndrome.

Laboratory Investigations - Do CT soon - CT shows blood in 95% of subarachnoid hemorrhages on the day of the bleed, in 80% on day 5, in 50% on day 7. Most subarachnoid hemorrhages are from ruptured aneurysms, some are from AVMs, and others are of unknown etiology. Blood localized to the mesencephalic cisterns indicates a benign condition.

If CT is negative - Admit patient for LP, but delay the LP until at least 12 hours after headache onset to allow the RBCs to disintegrate to the pigments responsible for xanthochromia (yellowish color).

CSF analysis - Measure opening pressure. Count red and white blood cells. Note: The difference in the RBC count between the first and last tubes of collected CSF does not reliably distinguish subarachnoid hemorrhage from traumatic tap. Only the presence of xanthochromia makes this distinction.

Right after the CSF is collected, the physician should take the tubes to the lab. One tube should be centrifuged and its supernate compared with a tube containing water to determine whether it is colored (xanthochromic). Ideally, the supernate should be analyzed in a spectrophotometer (not done here).

If the CSF pressure is elevated (above 200 mm) without evidence of subarachnoid hemorrhage, consider cerebral venous sinus thrombosis, even in the absence of cerebral signs such as a seizure, hemiparesis, or stupor, and perform MRI/MRA or catheter angiography.

Non-thunderclap acute severe new headache Differential diagnosis Subarachnoid hemorrhage, meningitis, encephalitis, subdural hematoma, tumor, migraine, unruptured cerebral aneurysm, cerebral venous sinus thrombosis, and dissection of a carotid or vertebral artery.

Laboratory Investigations - Do CT first to look for blood (see above), tumor, or hematoma.

If no blood or mass are present, do LP to look for evidence of subarachnoid blood (see above) or infection (WBC, protein, glucose, bacterial and fungal stains and cultures). Don't culture fluid or request stains in the absence of pleocytosis. Do measure the opening pressure, for a clear elevation without evidence of bleeding into the subarachnoid space or infection may indicate the presence of a cerebral venous sinus thrombosis.

If these studies are negative, the diagnosis is generally migraine.

Acute severe recurrent headaches seen in the Emergency Room (ER) Most are migraines. Some are analgesic-abuse headaches. Some are cluster headaches. A small percentage are feigned to obtain opiates (narcotics)

Treatment of migraine in the ER The most logical first treatment would be to inject 6 mg of sumatriptan subcutaneously if it hasn't been used previously or if it has been helpful before but not taken for the current attack, if no contraindications exist.

If sumatriptan has not been helpful in the past, the next best step would be to inject 1 mg of dihydroergotamine (DHE) IV by slow push (~10 minutes) or infuse it from a bag containing 50 ml of D5W, if no contraindications exist and if the drug has not been unsuccessful in the past. Preceding this with an IV infusion of 10 mg of metoclopramide is generally helpful in preventing or ameliorating DHE-induced nausea. When a migraine has been severe for 2-3 days or more, patients may need admission for several DHE infusions given at 6-hour intervals. If 1 mg doses give side effects, then smaller doses should be given.

The results of an open-label, pilot study by Wang et al. (1997) suggest that droperidol (a butyrophenone related to haloperidol) might be a potent reliever of refractory migraine attacks and status migrainosus (attacks lasting more than 72 hours). Hence, this drug should be a good choice for patients for whom injected sumatriptan or DHE are contraindicated or ineffective. The dose used in the study was 2.5 mg IV push (one minute injection) every 30 minutes until either three doses had been given or the patient was markedly relieved. Because of the high incidence of akathisia and the small incidence of dystonic reactions following droperidol, oral diphenhydramine is recommended after the completion of the therapy. Success has also been reported with other neuroleptics, namely chlorpromazine, 25-50 mg IM, or prochlorperazine, 10 mg IV.

Very recently, an uncontrolled, unblinded study of intravenous valproate sodium by Mathew, Kailasam, et al. (2000) suggested that this therapy aborts migraine headaches rapidly in most patients. 66 attacks in 61 patients who presented to the Houston (Texas) Headache Clinic with moderate to severe migraine headache (with or without aura) were infused intravenously with 300 mg of valproate sodium dissolved in 100 ml of normal saline. The mean infusion time was 10 minutes. 73% of the patients felt that the treatment gave "significant" relief: a reduction of pain from severe or moderate to mild or none, or a 50% reduction in headache intensity even though moderate headache persisted. Relief was judged at 30 minutes after the start of the infusion. If these results prove true, then this therapy would be especially suitable for patients for whom injected sumatriptan or DHE are ineffective or contraindicated.

IM injection of 100 mg meperidine mixed with 50 mg hydroxyzine usually dulls the pain, but is generally less effective than the above.

A quiet dark room, ice packs for the head, and sedation are generally helpful ancillary measures. http://www.upstate.edu/neurology/haas/


\5 heartburn (reflux)

Gastroesophageal reflux disease (GERD) is a digestive disorder that affects the lower esophageal sphincter (LES)--the muscle connecting the esophagus with the stomach. Many people, including pregnant women, suffer from heartburn or acid indigestion caused by GERD. Doctors believe that some people suffer from GERD due to a condition called hiatal hernia. In most cases, heartburn can be relieved through diet and lifestyle changes; however, some people may require medication or surgery. This fact sheet provides information on GERD-its causes, symptoms, treatment, and long-term complications.

What Is Gastro-esophageal Reflux? Gastroesophageal refers to the stomach and esophagus. Reflux means to flow back or return. Therefore, gastroesophageal reflux is the return of the stomach's contents back up into the esophagus. In normal digestion, the LES opens to allow food to pass into the stomach and closes to prevent food and acidic stomach juices from flowing back into the esophagus. Gastroesophageal reflux occurs when the LES is weak or relaxes inappropriately allowing the stomach's contents to flow up into the esophagus. Fig 1 shows the location of the LES between the esophagus and the stomach. The severity of GERD depends on LES dysfunction as well as the type and amount of fluid brought up from the stomach and the neutralizing effect of saliva.

What Is the Role of Hiatal Hernia? Some doctors believe a hiatal hernia may weaken the LES and cause reflux. Hiatal hernia occurs when the upper part of the stomach moves up into the chest through a small opening in the diaphragm (diaphragmatic hiatus). The diaphragm is the muscle separating the stomach from the chest. Recent studies show that the opening in the diaphragm acts as an additional sphincter around the lower end of the esophagus. Studies also show that hiatal hernia results in retention of acid and other contents above this opening. These substances can reflux easily into the esophagus.

Coughing, vomiting, straining, or sudden physical exertion can cause increased pressure in the abdomen resulting in hiatal hernia. Obesity and pregnancy also contribute to this condition. Many otherwise healthy people age 50 and over have a small hiatal hernia. Although considered a condition of middle age, hiatal hernias affect people of all ages. Hiatal hernias usually do not require treatment. However, treatment may be necessary if the hernia is in danger of becoming strangulated (twisted in a way that cuts off blood supply, i.e., paraesophageal hernia) or is complicated by severe GERD or esophagitis (inflammation of the esophagus). The doctor may perform surgery to reduce the size of the hernia or to prevent strangulation.

What Other Factors Contribute to GERD? Dietary and lifestyle choices may contribute to GERD. Certain foods and beverages, including chocolate, peppermint, fried or fatty foods, coffee, or alcoholic beverages, may weaken the LES causing reflux and heartburn. Studies show that cigarette smoking relaxes the LES. Obesity and pregnancy can also cause GERD.

What Does Heartburn Feel Like? Heartburn, also called acid indigestion, is the most common symptom of GERD and usually feels like a burning chest pain beginning behind the breastbone and moving upward to the neck and throat. Many people say it feels like food is coming back into the mouth leaving an acid or bitter taste. The burning, pressure, or pain of heartburn can last as long as 2 hours and is often worse after eating. Lying down or bending over can also result in heartburn. Many people obtain relief by standing upright or by taking an antacid that clears acid out of the esophagus. Heartburn pain can be mistaken for the pain associated with heart disease or a heart attack, but there are differences. Exercise may aggravate pain resulting from heart disease, and rest may relieve the pain. Heartburn pain is less likely to be associated with physical activity.

How Common Is Heartburn? More than 60 million American adults experience Gerd and heartburn at least once a month, and about 25 million adults suffer daily from heartburn. Twenty-five percent of pregnant women experience daily heartburn, and more than 50 percent have occasional distress. Recent studies show that GERD in infants and children is more common than previously recognized and may produce recurrent vomiting, coughing and other respiratory problems, or failure to thrive.

What Is the Treatment for GERD? Doctors recommend lifestyle and dietary changes for most people with GERD. Treatment aims at decreasing the amount of reflux or reducing damage to the lining of the esophagus from refluxed materials. Avoiding foods and beverages that can weaken the LES is recommended. These foods include chocolate, peppermint, fatty foods, coffee, and alcoholic beverages. Foods and beverages that can irritate a damaged esophageal lining, such as citrus fruits and juices, tomato products, and pepper, should also be avoided. Decreasing the size of portions at mealtime may also help control symptoms.

Eating meals at least 2 to 3 hours before bedtime may lessen reflux by allowing the acid in the stomach to decrease and the stomach to empty partially. In addition, being overweight often worsens symptoms. Many overweight people find relief when they lose weight. Cigarette smoking weakens the LES. Therefore, stopping smoking is important to reduce GERD symptoms. Elevating the head of the bed on 6-inch blocks or sleeping on a specially designed wedge reduces heartburn by allowing gravity to minimize reflux of stomach contents into the esophagus.

Antacids taken regularly can neutralize acid in the esophagus and stomach and stop heartburn. Many people find that nonprescription antacids provide temporary or partial relief. An antacid combined with a foaming agent such as alginic acid helps some people. These compounds are believed to form a foam barrier on top of the stomach that prevents acid reflux from occuring. Long-term use of antacids, however, can result in side effects, including diarrhea, altered calcium metabolism (a change in the way the body breaks down and uses calcium), and buildup of magnesium in the body. Too much magnesium can be serious for patients with kidney disease. If antacids are needed for more than 3 weeks, a doctor should be consulted. For chronic reflux and heartburn, the doctor may prescribe medications to reduce acid in the stomach. These medicines include H2 blockers, which inhibit acid secretion in the stomach.

Currently, four H2 blockers are available: cimetidine, famotidine, nizatidine, and ranitidine. Another type of drug, the proton pump (or acid pump) inhibitor omeprazole inhibits an enzyme (a protein in the acid-producing cells of the stomach) necessary for acid secretion. The acid pump inhibitor lansoprazole is currently under investigation as a new treatment for GERD. Other approaches to therapy will increase the strength of the LES and quicken emptying of stomach contents with motility drugs that act on the upper gastrointestinal (GI) tract. These drugs include bethanechol and metoclopramide.

Tips To Control Heartburn Avoid foods and beverages that affect LES pressure or irritate the esophagus lining, including fried and fatty foods, peppermint, chocolate, alcohol, coffee, citrus fruit and juices, and tomato products. Lose weight if overweight. Stop smoking. Elevate the head of the bed 6 inches. Avoid lying down 2-3 hrs after eating. Take an antacid.

What If Symptoms Persist? People with severe, chronic esophageal reflux or with symptoms not relieved by the treatment described above may need more complete diagnostic evaluation. Doctors use a variety of tests and procedures to examine a patient with chronic heartburn. An upper GI series may be performed during the early phase of testing. This test is a special x-ray that shows the esophagus, stomach, and duodenum (the upper part of the small intestine).

While an upper GI series provides limited information about possible reflux, it is used to rule out other diagnoses, such as peptic ulcers. Endoscopy is an important procedure for individuals with chronic GERD. By placing a small lighted tube with a tiny video camera on the end (endoscope) into the esophagus, the doctor may see inflammation or irritation of the tissue lining the esophagus (esophagitis). If the findings of the endoscopy are abnormal or questionable, biopsy (removing a small sample of tissue) from the lining of the esophagus may be helpful. The Bernstein test (dripping a mild acid through a tube placed in the mid-esophagus) is often performed as part of a complete evaluation.

This test attempts to confirm that the symptoms result from acid in the esophagus. Esophageal manometric studies-pressure measurements of the esophagus-occasionally help identify critically low pressure in the LES or abnormalities in esophageal muscle contraction. For patients in whom diagnosis is difficult, doctors may measure the acid levels inside the esophagus through pH testing. Testing pH monitors the acidity level of the esophagus and symptoms during meals, activity, and sleep. Newer techniques of long-term pH monitoring are improving diagnostic capability in this area.

Does GERD Require Surgery? A small number of people with GERD may need surgery because of severe reflux and poor response to medical treatment. Fundoplication is a surgical procedure that increases pressure in the lower esophagus. However, surgery should not be considered until all other measures have been tried.

What Are the Complications of Long-Term GERD? Sometimes GERD results in serious complications. Esophagitis can occur as a result of too much stomach acid in the esophagus. Esophagitis may cause esophageal bleeding or ulcers. In addition, a narrowing or stricture of the esophagus may occur from chronic scarring. Some people develop a condition known as Barrett's esophagus, which is severe damage to the skin-like lining of the esophagus. Doctors believe this condition may be a precursor to esophageal cancer.

Conclusion Although GERD can limit daily activities and productivity, it is rarely life-threatening. With an understanding of the causes and proper treatment most people will find relief.

Indigestion, also known as upset stomach or dyspepsia, is a painful or burning feeling in the upper abdomen, often accompanied by nausea, abdominal bloating, belching, and sometimes vomiting. Indigestion might be caused by a disease or an ulcer in the digestive tract, but for most people, it results from eating too much, eating too quickly, eating high-fat foods, or eating during stressful situations. Smoking, drinking too much alcohol, using medications that irritate the stomach lining, being tired, and having ongoing stress can also cause indigestion or make it worse.

Some people have persistent indigestion that is not related to any of these factors. This type of indigestion--called functional or nonulcer indigestion--is caused by a problem in how food moves through the digestive tract. To diagnose indigestion, the doctor first rules out other problems, like ulcers. In the process of diagnosis, a person may have x-rays of the stomach and small intestine or undergo endoscopy, in which the doctor uses an instrument to look closely at the inside of the stomach. Avoiding the foods and situations that seem to cause indigestion is the most

successful way to treat it. Excess stomach acid does not cause or result from indigestion, so antacids are not an appropriate treatment, although some people report that they do help. Smokers can help relieve their indigestion by quitting smoking, or at least not smoking right before eating. Exercising with a full stomach may cause indigestion, so scheduling exercise before a meal or at least an hour afterward might help. To treat indigestion caused by a functional problem in the digestive tract, the doctor may prescribe medicine that affects stomach movement.

Because indigestion can be a sign of or mimic a more serious disease, people should see a doctor if they have Vomiting, weight loss, or appetite loss. Black tarry stools or blood in vomit. Severe pain in the upper right abdomen. Discomfort unrelated to eating. Indigestion accompanied by shortness of breath, sweating, or pain radiating to the jaw, neck, or arm.

\6 Lupus

is systemic, and falls into a large group of conditions called autoimmune disorders. That means your immune system is attacking some of your own tissues. Your antibodies and immune cells, such as your white cells, are supposed to attack only foreign subs tances, bacteria and viruses. In autoimmune disorders, these foot soldiers turn on their own army, and the civilians, too. It's kind of like "friendly fire." The big, globular proteins called antibodies that float around in our blood start going after ou r own cells, which often causes anemia and low levels of white cells and platelets. These antibodies also glob on to lots of other proteins and create huge floating nasty bits called immune complex. These highly reactive protein chunks get stuck in the t iniest blood vessels, the capillaries, and cause the heavy cruisers, the white cells, to be called in. This results in inflammation and breakdown of tissues in places like the skin, the kidneys, the joints and any mucous membrane.

The most common symptoms of lupus are fever, anorexia, malaise, weight loss, facial rash (particularly with exposure to sunlight), hair loss and joint pain. Lupus can be caused by certain medications like procainamide, hydralazine and isoniazid. Women in their child-bearing years make up 85 percent of lupus patients. There can be a family association with this disease, but for most people who get lupus, there is no family history of sufferers. The diagnosis is made by laboratory tests, and the best specialist to see is a rheumatologist.

Lupus tends to go through cycles getting worse, than getting better again. Some people can get away with little or no treatment, but others may need to be on a regular schedule of medications. The first thing most people get from their doctors is a nonst eroidal anti-inflammatory med, or one of the new Cox-2 inhibitors, Celebrex or Vioxx. During the bad times, doctors usually like to use some pretty big pharmaceutical guns, like corticosteroids and immunosuppressive drugs. These drugs may improve the pro gnosis for people with lupus, but there are some other steps you can take that may decrease your need to use this heavy artillery.

Diet is critical. There is good evidence that a low-fat diet with adequate essential fatty acids may dramatically decrease overall inflammation. Stay away from animal fats and grease in general. Here's why: There's a whole group of compounds in the body  called prostaglandins. Some regulate how easily our blood clots and, generally, how inflamed we are. The body makes animal fats into prosta-glandins, and that increases inflammation and blood clotting. Fish fats, on the other hand, are made into an anti- inflammatory type of prostaglandins, so  you guessed it  eat fish. The oil in deep water fish like tuna, salmon, sardines, mackerel and trout contain Omega-3 fats, which produce this effect. Substitute fresh vegetables, fruits and these light fish prot eins for the double egg chili cheeseburgers.

What about supplements? Well, if you really can't stand any kind of fish, you can get an effect that's almost as good by taking fish oil capsules. (These are sometimes called EPA/DHA after the names of the actual fatty acids.) Without dietary help, 12 to 18 fish oil capsules a day may help you. If you're eating a low-fat diet, you may need only eight to 10 capsules a day.

In the same group of compounds is gamma linolenic acid. This anti-inflammatory compound has been widely studied  one study showed that taking 1.4 grams of this substance each day reduced the number of tender joints by 36% and the number of swollen joint s by 48%. Sounds like a good weapon to have on your side.

Dietary antioxidants may also help. There's some evidence that vit E, vit C, quercetin, beta-carotene, selenium and other minerals have the ability to reduce chemical stress and also have anti-inflammatory properties. (Don't try to get a dose of each of  these individually; take a daily multivitamin and multi-mineral tablet instead.) Quercetin is a plant extract that has been shown to inhibit the formation of the bad prostaglandins and impede the release of the inflammatory substance histamine.

Similarly, some herbal therapies may help. Turmeric, also called curcumin, is a spice used often in Indian food. It's also used in Ayurvedic medicine as an anti-inflam-matory. Some studies have shown that 1,200 milligrams per day produce significant impr ovement in morning stiffness of joints, and in the physical endurance of patients with inflammatory conditions. Bromelain, a compound extracted from pineapple, has been shown to decrease joint pain and morning stiffness, and increase range of motion. It' s usually given in doses of 1 to 2 grams per day. There are a few other herbal remedies that are being investigated at this time, so keep your eye out for more on this.

Even the most conservative med textbooks emphasize the need for emotional support if you've got an autoimmune disorder. Most people will feel helpless upon hearing that the diagnosis. This is to be expected; sometimes the feeling of helplessness may be m ore disabling than the disease itself. Physicians often recommend counseling, and nearly always recommend the support of the patient's family and friends. I would add that anyone with lupus or another serious illness should explore his or her own approac hes for dealing with the stress the condition causes. The mind/body connection is profound, and even the most conventional physicians understand this.

This is a lot to take in. You may be wondering what you should do first. Well, if I had just received a diagnosis of lupus, there are a handful of things that I would start with. The whole idea is to keep inflammation as low as possible, so you won't hav e to use the heavy drugs with the big side effects very often. First, I would make sure that my diet was as good as it can be. I would be sure to take a good multivitamin and multi-mineral supplement every day. I would probably take a supplement with gamma linolenic acid and quercetin. I would learn to cook with plenty of turmeric on a regular basis. I would meditate daily, manage my stress as best I could, and take yoga classes.

Beyond that, I would find the best rheumatologist that I could, and get regular checkups. There are always new treatments in the pipeline. This is not a losing battle, just an ongoing challenge. I wish you the best of luck.


\7 blood pressure, hypertension

Blood pressure readings are usually given as two numbers: 110 over 70 (written as 110/70). The first number is called the systolic blood pressure reading and represents the maximum pressure exerted when the heart contracts. The second number (the lower number) is called the diastolic blood pressure reading and it represents the pressure in the arteries when the heart is at rest.

HBP - high blood pressure Definition: Increased or elevated blood pressure, either intermittent or sustained, exceeding 140/90 mmHg (millimeters of mercury).

Considerations: About 1 in every 5 adults in the U.S. has high blood pressure. Elevated blood pressure occurs more often in men than in women and in African Americans almost twice as often as in Caucasians.

Hypertension can affect all types of people. Most people feel no symptoms with uncomplicated high blood pressure. Essential hypertension (hypertension with no known cause) is not fully understood but accounts for about 85% of all hypertension cases in people over 45 years of age.

Even though many high blood pressure cases do not have a known cause, the condition can still be treated effectively. There are dozens of different medications available for the management of high blood pressure.

Common causes: medications (such as appetite suppressants) habitual alcohol use excess sodium (salt) in diet obesity anxiety or stress arteriosclerosis agitation coarctation of the aorta immobilization pain acute tubular necrosis hemolytic-uremic syndrome Henoch-Schonlein purpura periarteritis nodosa radiation enteritis renal artery stenosis retroperitoneal fibrosis fibromuscular dysplasia Wilms' tumor hydronephrosis renal aphasia renal vein thrombosis renal artery embolism renal artery occlusion glomerulonephritis (see individual types) amyloidosis diabetes mellitus gout nephrolithiasis idiopathic neuropathy

obstructive uropathy (see individual diseases) drugs such as alcohol toxicity, anesthesia, antianxiety agents, antihypertensives, calcium channel blockers, diuretics, general anesthetics, antiarrhythmics, monoamine oxidase inhibitors, narcotic analgesics, tranquilizers, and vasodilators

Note: There may be other causes of high blood pressure. This list is not all inclusive, and the causes are not presented in order of likelihood. The causes of this symptom can include unlikely diseases and medications. Furthermore, the causes may vary based on age and gender of the affected person, as well as on the specific characteristics of the symptom such as time course, aggravating factors, relieving factors, and associated complaints. Use the Symptom Analysis option to explore the possible explanations for high blood pressure, occurring alone or in combination with other problems.

Blood pressure is pressure in the arteries as the heart pumps blood around the body. What to look for There are generally no symptoms for high blood pressure as the early stages of hypertension may take a few years to develop A higher than normal blood pressure. Normal for young and middle aged adults is a pressure of 120/80. A pressure of 140/90 is definitely something to be concerned about. If the pressure is 160/95 it requires treatment. Blackouts, a minor stroke are indications that your blood pressure is too high and can be fatal if it is not treated. swollen ankles shortness of breath headaches, dizziness and nose bleeds

Traditional Treatment Your doctor will give you a thorough examination to check if your blood pressure is the result of another disease such as Cushings disease or kidney problems however, usually there is no immediate cause for the high blood pressure. It is advisable that if over weight, the patient try to stay within your recommended weight level. Also try to avoid salt in your diet and reduce stress levels in your lifestyle. Exercise is also recommended. If you have a stressful job, some doctors will advise you to give it up and take some time off to rest completely.

These lifestyle changes quite often bring the blood pressure down considerably. A doctor will prescribe medication for you if the above approaches and lifestyle changes still do not bring the blood pressure down. Some of these drugs will have side effects which can be serious. Your doctor will know which drugs should be given to you and will explain all the side effects to you. The doctor will keep a close check on the patient to take the blood pressure and watch for possible side effects.

Alternative/Natural Treatments Body/Mind Work - Yoga, Meditation and other relaxation techniques can help relax the patient and lower the stress levels.

Herbal Remedies - Hawthorn, dandelion and linden, garlic and ginger are helpful for blood pressure problems. Hawthorn, dandelion and linden, garlic and ginger are helpful for blood pressure problems.

Dietary Considerations Eat less salt - best of all try to avoid it altogether (use herbs, garlic and ginger instead) Avoid heavily salted food (such as packaged food) Try to eat more dairy products - low fat one only. You may be low on calcium.

Avoid too much alcohol as this can raise blood pressure. Give up smoking as this can harden the arteries and cause coronary heart disease. When to seek further professional advice if your blood pressure is over the recommended level if you have any of the symptoms listed above if you are on medication for high blood pressure and are suffering any side effect - see your doctor immediately.

HIGH BLOOD PRESSURE also called hypertension, is a common cardiovascular disorder, often with no symptoms, in which the blood exerts an abnormal amount of force on the inside walls of the arteries persistently. This sustained pressure increases the risk of other serious disorders, such as stroke, heart attack, and kidney failure. Although more than 50 million Americans have high blood pressure, only about half of them are aware of it.

As the heart pumps, it pushes blood into the arteries with just enough force to keep it flowing forward. The arteries carry the oxygen- and nutrient-rich blood to all the bodys tissues and organs. Blood pressure is the force of the blood pushing against the walls of those arteries. Blood pressure readings consist of two numbers: the systolic pressure, the amount of force exerted within the arteries while the heart is actively pumping or contracting (the first or top number); and the diastolic pressure, the force exerted when the heart is at rest in between each beat (the second or bottom number). These pressures are measured in millimeters of mercury (mm Hg), in other words, a pressure of 100 mm Hg means that the force within the arteries can raise a column of mercury 100 mm on a blood pressure measuring instrument called a sphygmomanometer.

A normal blood pressure taken when the person is at rest averages around 120/70, but a wide range of occasional fluctuations is expectedwith exercise, stress, or changes in position, for example. That is why it usually takes several readings to confirm that a person actually has high blood pressure, defined as either a systolic pressure consistently at 140 mm Hg or higher or a diastolic pressure consistently at 90 mm Hg or higher. Consistently high blood pressure forces the heart to work extra hard to pump blood, and can also deprive other organs and systems of essential nutrients. Left untreated, high blood pressure can lead to:

An enlarged heart. If the heart has to work harder and longer, it tends to get bigger just like any other muscles that must carry a heavy load. Eventually the heart muscles stretch too much or get too thick, and the heart cannot pump enough blood to meet the bodys needs. It no longer functions efficiently, blood is not pumped forward into the rest of the body, and the heart eventually fails. A stroke. As the blood pressure in the brain increases, the lining of the inner walls of the blood vessels becomes damaged, much like an overinflated tire develops weak or rough spots. The stressed blood vessels can develop aneurysmsweak or thin spots that can balloon out and eventually burst. Or, cholesterol, calcium, and other cellular debris can "catch" on rough spots, forming plaque and clogging arteries (a condition called atherosclerosis, or hardening of the arteries). When an aneurysm ruptures or blood cant get through clogged arteries, the blood that is supposed to nourish brain tissues never reaches its destination. Starved for nutrients, those tissues die, and the person has a stroke. Paralysis and loss of body function and motor skills are the result. Kidney failure. Continued high blood pressure reduces the supply of nutrients to the kidneys, eventually damaging them. Once the kidneys can no longer filter out enough fluid and waste products, they build up in the body. Eventually, the person needs dialysis to do the work the kidneys can no longer do. A heart attack. If one of the arteries nourishing the heart closes off due to atherosclerosis, portions of the heart muscle are damaged and the person has a heart attack. Loss of vision. High blood pressure can cause blood clots or ruptures in tiny blood vessels in the retina, leading to reduced vision or blindness.

In 95% of the people who have high blood pressure, the cause is unknown. That type of high blood pressure is called primary or essential hypertension. In the remaining cases, high blood pressure is considered secondary, caused by kidney disease, oral contraceptives, pregnancy, hormone imbalances, tumors of the adrenal glands, or some other abnormality.

The following risk factors for high blood pressure have been identified:

family history diabetes mellitus stress physical inactivity race (with African-Americans at highest risk) sex (with men at higher risk than women) age (over 35) obesity salt sensitivity excessive alcohol consumption

SIGNS AND SYMPTOMS Most people with high blood pressure have no symptoms, but with severe elevations in blood pressure, the following are possible:

headache drowsiness and confusion numbness and tingling in the hands and feet coughing up blood nosebleeds shortness of breath ringing in the ears palpitations

DETECTION AND DIAGNOSIS Since most people with high blood pressure have no symptoms, the doctor usually discovers high blood pressure during a routine physical examination, or an exam for some other problem. Blood pressure is taken by wrapping a cuff attached to a sphygmomanometer around the upper arm and inflating the cuff with air to stop the blood flow in the artery for a few seconds. The doctor or nurse slowly opens the valve to deflate the cuff, while listening with a stethoscope to the sounds of blood rushing through an artery in the same arm. The reading on the mercury column at the moment the first sound is heard is the systolic pressure. The reading at the last sound is the diastolic pressure. Several readings might have to be taken at different times and with the patient relaxed and at rest to confirm high blood pressure. (Often the stress of seeing the doctor raises blood pressure, a phenomenon called "white coat hypertension.") Readings are interpreted according to the following (or a similar) scale:

INTERPRETING BLOOD PRESSURE

Category

Systolic

Diastolic Optimal blood pressure under 120 mm Hg under 80 mm Hg

Normal blood pressure under 130 mm Hg under 85 mm Hg

High normal blood pressure 130-139 mm Hg 85-89 mm Hg

Stage 1: mild hypertension

140-159 mm Hg

90-99 mm Hg

Stage 2: moderate hypertension

160-179 mm Hg

100-109 mm Hg

Stage 3: severe hypertension 180-209 mm Hg 110-119 mm Hg

Stage 4: very severe hypertension 210 mm Hg or above 120 mm Hg or above

TREATMENT Unless blood pressure is especially high, the patient has symptoms, or the patient is at high risk for complications, most doctors recommend lifestyle changes before starting drug therapy. These changes include:

eating a nutritious, balanced diet low in salt and fat and high in fiber, calcium, and magnesium exercising regularly maintaining a weight appropriate for height, frame, age, and gender quitting smoking reducing alcohol consumption taking supplemental potassium, calcium, folic acid, and magnesium if the diet does not contain enough of these essentials practicing stress-relieving and relaxation techniques getting frequent blood-pressure checks

If lifestyle changes do not bring the patients blood pressure to safe levels consistently, the doctor will probably start drug therapy. There is a wide variety of drugs available for lowering blood pressure, and it may take some time to find the right approach for each individual patient.

Many doctors begin with diuretics (water pills) to help the body eliminate salt and water through urination, thereby reducing blood volume and pressure. Adrenergic blockers are another good initial choice. These drugs act by blocking the effects of the sympathetic nervous system, a network of nerves that respond to stress by raising blood pressure. Other options include angiotensin-converting enzyme (ACE) inhibitors, which lower blood pressure by dilating (opening up) the arteries; calcium-channel blockers, which relax blood-vessel walls, thereby lowering pressure; and vasodilators, which relax the smooth muscles of the arteries and reduce the resistance to blood flow.

PREVENTION Although essential hypertension cannot be prevented, it is a good idea for all adults, and especially those who have any risk factors for high blood pressure, to get regular blood pressure checks. Early detection means prompt treatment, including lifestyle changes (as described above) that might help keep blood pressure at safe enough levels to prevent complications. Prompt and thorough management of any medical conditions might in some cases help prevent secondary hypertension.

GLOSSARY OF MEDICAL TERMS adrenal glands: a pair of glands, each of which sits on top of a kidney, that secrete a variety of

hormones, some of which regulate the balance of salt and water in the body

arteries: blood vessels that transport blood from the heart to the rest of the body

cardiovascular: pertaining to the heart and the blood vessels, which work together to distribute blood and the oxygen and nutrients it carries throughout the body

diabetes mellitus: a disorder in which the body cannot process carbohydrates efficiently

dialysis: a medical procedure for filtering waste products from the blood of patients whose kidneys are not functioning adequately

retina: light-sensitive layer of the eyeball that receives images of objects and transmits corresponding impulses to the brain for interpretation

stethoscope: device for listening to body sounds, especially in the heart and lungs, with earpieces at one end and a bell that goes on the patients skin at the other end

This information is not intended to provide advice for individual problems, nor to substitute for professional advice or care from a physician. For answers to specific questions about your personal circumstances, you should consult your physician directly.

QUESTIONS TO ASK YOUR DOCTOR

What is a normal blood pressure?

What numbers do you consider dangerously high? At what point should I call you?

What do you think caused my high blood pressure? Is it due to stress? Could it be the result of kidney disease or some other problem?

What are my chances of having a stroke?

What is the best way to check my blood pressure? How often should it be checked?

Should I make changes in my diet?

How much should I exercise? What type of exercise is best for me?

HEART RATE MONITORS

CONTENTS Basic cardiovascular physiology Pros and cons of using a heart rate monitor Definitions Calculating your maximum heart rate Heart rate training zones Training tips using a heart rate monitor Resting heart rate An opposing opinion The Heart Rate Monitor (HRM) is touted by many cyclists and trainers as the most significant training advance in the last ten years. Although many coaches refuse to work with an athlete without the physiologic training info it provides, HRMs have their detractors. And that small backlash is slowly growing. An alternative to a HRM, not quite as technical and rigid, uses perceived effort as a measure of your level of exertion.

BASIC CARDIOVASCULAR PHYSIOLOGY First, let's review the basic physiology of the circulatory system asking ourselves the question "What does the heart rate really indicate?" The components of the cardiovascular system are: the heart (the pump) the arteries (a distribution system) the capillaries (the exchange system where gases, nutrients, and other chemical compounds move to and from surrounding tissue the veins (which are the return circuit) With every heart beat (contraction of the heart pump), a certain amount of blood (stroke volume) is pushed through the system. The contraction frequency of the heart is the heart rate (HR). The amount of blood moved to the cells of the body every minute is the product of the heart rate and stroke volume (HR x strove volume). With physical activity (exercise) more oxygen is required by the muscle cells, and the circulatory system responds by increasing the heart rate (and the cardiac output). With aerobic training, the actual amount of blood pumped per heart beat (stroke volume) increases and the efficiency of the exchange process at the capillary level improves. The result is a lower heart rate for any level of physical activity in the trained versus the untrained individual. Thus aerobic training benefits include: a lower resting heart rate a lower heart rate for any specific level of exertion as well as an increased exercise capacity for an individual's maximum heart rate. The training effect results when the heart muscle is "stressed" by an increase in cardiac output (just as muscles in the arms and legs respond to the stress of lifting free weights). As the cardiac output is directly proportional to the heart rate, a heart rate monitor (HRM) can be used to structure and monitor an aerobic training program. (For additional background see Basic Exercise Physiology - the cardiac system.) Let's look at the pros and cons on the use of a HRM. PROS AND CONS The ADVANTAGES of a HRM include its use: as a motivational tool - like a coach ; brings objectivity to a training program. to teach beginners to read their bodies and avoid anaerobic overtraining. to aid in doling out energy during time trialing or climbing, saving some for the final effort. to analyze race efforts and design a personalized training program. to spot overtraining (heart rate 10% higher than normal on awakening for several consecutive days). The DISADVANTAGES of a HRM are: its inconsistency - at the same heart rate you're not always putting out the same effort day to day. the lack of scientific support - there is no evidence training with a HRM improve competitive performance. too much data, esp with elaborate HRMs, with little agreement on how to use this information to improve training or performance. the lag time in heart rate response to a change in exertion - 15 to 30 sec lag with 2 to 3 min to stabilize at the new level of exertion. its incompatibility with group training. it distracts from dangerous road hazards. DEFINITIONS Here are some definitions you'll encounter in the literature on heart rate monitors: bpm - beats per minute Max HR (MHR) - maximum heart rate (expressed in beats per minute) target heart rate - the training heart rate (usually a range of values) anaerobic threshold (AT)* (synonomous with lactate threshold). Lactate production occurs with muscle cell activity and increases as activity becomes more vigorous. Lactic acid is metabolized by the muscle cells, but at some point they cannot eliminate (or oxidize) the lactate as fast as it is being produced and the blood lactate level begins to increase. In trained athletes, this threshold for lactate buildup occurs at a higher activity level or percentage of the athlete's MHR or aerobic capacity. For all practical purposes, the AT is the highest heart rate you can maintain for a race or hard ride lasting up to an hour. As the AT increases with aerobic conditioning, it is considered one of the standard measurements to track training. The AT is usually reached at 80-90% of your maximum heart rate, but in elite riders rises to 90-93% of their maximum heart rate.(See also Basic Exercise Physiology - measures of cardiovascular fitness.) lactate threshold (LT). See anaerobic threshold. * Determining your actual Anaerobic Threshold (synonyms are lactate threshold, AT, LT, Concini test). Accurate laboratory determination of your anaerobic threshold requires frequent blood draws while pedaling an ergometer at steadily increasing workloads. But for training purposes, the following approach is an alternative. Using a single gear, start cycling at 35 kph. Slowly increase speed on a flat course by 1km/hr every 300 meters (1/5 mile). Chart heart rate vs speed. Anaerobic Threshold is the "breakpoint" where heart rate levels off relative to speed. Let's assume you have decided to use a heart rate monitor in your training program. The first step is calculating your MHR or maximum heart rate. CALCULATING YOUR MAXIMUM HEART RATE (MHR): Just as we all vary in height and body habitus, everyone has their own personal maximum heart rate genetically "hardwired". Our maximum heart rate also decreases approximately one bpm (beat per minute) per year. The average MHR of a teenager is 220 beats per minute, but this may vary +/- 11 beats from the average (209-231 bpm). For example, a 40 year old who would be expected to have a MHR of 180 (220-40) could vary from 169 to 191 for his or her own personal MHR. Another key point is maximum heart rates are "sport specific" i.e. they vary from one sport to another. For a given rate of oxygen consumption, weight bearing activities such as running raise the heart rate more than cycling (part of your weight is supported by the bike). So you cannot use your maximum heart rate from running to plan a cycling training program without risking overtraining. One of the following two approaches can be used to determine your MHR for cycling. The first is more accurate and the one I prefer. There can be marked discrepancies between the estimated MHR and real life results (up to 5% of the population can have heart rates 20 beats above or below the ESTIMATED figure). And if you are in shape, the typical decline of one beat per minute per year doesn't always hold. Warm up thoroughly. On a long, steady hill increase effort every minute for at least 5 minutes until you can't go any faster. Then sprint for 15 seconds. Check your heart rate at its maximum for a full 30 seconds and double the number. Similar results can be obtained on a stationary trainer. 220 minus your age in years. A rough figure and much less accurate than the on bike approach. The only limit to the length of time one can ride at 100% of their MHR is personal discomfort. This level of activity does not "strain" the heart muscle or have other harmful effects on the heart itself. Although this level of activity might be considered in a competitive race or event for a short sprint, maximizing the benefits of a training program is the result of a mixture of recovery and hard days (see below). As the time you can hold 100% MHR is considerably shorter than the time you can ride at 84-90% MHR, the art of racing is finding the right mix to get you to the finish line first. Most competitive athletes train at their lactate threshhold (84-90% of their MHR). HEART RATE TRAINING ZONES There are 5 training "zones" or heart rate ranges. These are arbitrary divisions and can differ from article to article or coach to coach. They are based on the increase in heart rate (and cardiac output) as the oxygen consumption of the exercising muscle increases, and the concept of the benefits of variable stress in developing the exercising muscle (heart or skeletal). As one moves up the hierarchy of training zones, exercise intensity increases and there is a shift from the use of fat as an energy source for the muscle cell to carbohydrate (below 70% MHR fat is burned preferentially). And as the MHR is reached, there is a shift in the muscle cell towards anaerobic (without oxygen) metabolism with increased lactic acid production. The Heart Rate Intensity Zones are divided as follows: Zone 1 65% of MHR (recovery rides) Zone 2 65-72% of MHR (endurance events) Zone 3 73-80% of MHR (high level aerobic activity) Zone 4 84-90% of MHR (lactate threshold(LT,AT); time trialing) Zone 5 91-100% of MHR (sprints and anaerobic training) If you always train at low heart rates, you will develop endurance with no top end speed. Conversely if you train hard most of the time, you'll never recover completely and chronic fatigue will poison your performance. The solution is to mix hard training with easy pedaling in the proper proportions. The best approach is to stay below 80% of maximum heart rate (zones 1 to 3) on your easy days to build an aerobic base while allowing day to day recovery, and then push above 85% when it's time to go hard to improve your high level performance. But avoid training in the no man's land or mediocre middle at
80-85% of MHR where it's too difficult to maintain the pace for the long rides needed to build endurance and allow some recovery time, but not hard enough to significantly improve your aerobic performance and increase your lactate threshold. Training programs should be individualized, but once a good base is developed early in the season with Zones 1 and 2 exertion, most programs contain the following elements.

TRAINING TIPS USING A HEART RATE MONITOR

Tips for a training week: (see also mileage tips and training options) one long recovery ride - zone 1 or 2 one long day (event distance + 10 to 20%) - maxhr = to that planned for the event three high intensity days - zone 4 one or two interval workout days which are counted as one of the three zone 4 days. For example: warm up - zone 1 20 min - zone 3 5 min - zone 4 7 intervals - hit 90% max, recover to 60 - 65% max 5 min - zone 4 20 min - zone 3 warm down - zone 1 the sixth and seventh days of the week can be rest days off the bike or slow recovery rides at zone 1 or 2 exertion to stretch out your muscles.

RESTING HEART RATE Your resting heart rate (RHR) can also be used as an indicator of your degree of training. As you train, your resting heart rate will fall. This is a result of the increased efficiency of the circulatory system. The heart will increase the volume of blood pumped per beat, and the peripheral muscle cells will become more effective at extracting oxygen from the blood passing through their capillary networks. The RHR for an untrained individual is 60 to 80 beats per minute. With training, it is not uncommon to see the RHR fall into the high 40s or low 50s. And as mentioned above, regular monitoring of your resting heart rate in the mornings (before getting up and beginning your daily activities) can be used as a monitor for overtraining (heart rate on awakening and before getting out of bed 10% higher than your personal normal for several consecutive days). AN OPPOSING OPINION But there are differences of opinion on the usefulness of a heart rate monitor for training and competing. So keep an open mind and don't consider the HRM as the only real key to success. The following is from an Aussie coach, Graham Fowler: "I have observed a number of different %max heart rates during time trials. My nephew once rode a junior nationals ITT at 100%MHR. He didnt win it needless to say however didnt crack either. Obviously he was very fit or his MHR was inaccurate. I advise riders to ride just above (1 to 5 beats per min) what they consider threshold. This is around 92%mhr. This mark needs to be derived in training. I am aware of race day anxiety causing the heart rate to elevate somewhat so the hr is not such a good measure with an anxious rider. I am more inclined in the future the train with heart rate to establish a perceved effort (pe), and then remove the heart rate meter during racing and ride on pe alone. The speedo is then the govener (sic)."

Stretching With exercise there is microscopic injury to muscle tissue, and the more vigorous the activity or the more it exceeds your level of training, the greater that injury. This injury occurs in muscles which are actively contracting (your quads for example) as well as in muscles being held in a constant state of contraction (isometric) for long periods of time (such as your shoulder muscles on a long ride). Microscopic muscle injury is one of the reasons for why you get sore muscles after a vigorous workout or competition. This microtrauma will cause the tissue to swell (edema) with an influx of inflammatory cells, and in the healing phase, there can be development of fibrous or scar tissue. During the initial inflammatory phase of this process the muscle responds with a reflex spasm which is the tightness or knot you can feel. Stretching or massage (where someone else is stretching the muscle in question for you) can help to relax this muscle spasm and minimize edema with subsequent fibrous tissue formation. And there is some evidence that a muscle that has been fully lengthened (stretched) before activity will contract more forcefully and improve performance. It is important to stretch only after the muscle to be stretched has been actively warmed up - either with 5 or 10 minutes of exercise or in the post exercise period. There is scientific evidence that this will increase tissue elasticity and ductility, and reduce the frequency of injuries directly related to the stretching itself. Does stretching done after the warmup period decrease the incidence of injury from the subsequent activity? That is unproven at this point, but common sense would suggest that if the muscle edema and spasm are minimized, there should be less stress on the muscle fibers and thus less additional injury. For cyclists, the most common muscles requiring post exercise stretching or massage are the hamstrings, quadriceps, and shoulder muscles. As an inflamed muscle, or one in spasm, is uncomfortable to pressure, it is easy for you to identify your own areas of overuse. When massaging a muscle, two approaches can be used. First is to apply pressure on the area of discomfort (the palpable knot) with the muscle in a neutral, relaxed position. The pressure is then moved along the direction of the muscle fibers (remember to massage in the direction of the muscle fibers - the direction of pull of the muscle) to counteract the spasm and "work out" the pain. Over the last few years, there has been increased interest in "active" strecting or massage which means that steady pressure is maintained on the tender area or muscle, and the extremity is actively put through it's range of motion, contracting and moving the muscle beneath the point of pressure. The theory being that this involves the nerve/muscle unit and may retrain the entire motor unit to sustain a decrease in spasm after the massage session has been completed. What can you do to maximize the benefits of a stretching program? keep a training diary that includes notation of muscle soreness that might need extra stretching or massaing later, particularly if there is a trend over several days/weeks. stretch for long enough - I've heard the recommendation of 2 minutes of active stretching (that means keeping the muscle on stretch tension) for every 15 minutes of vigorous exercise. This was for track competitiors and may be less for those biking many hours a day for their training. But the idea is that you can't overdo on the time devoted to stretching. be sure to adequately hydrate during your exercise.


\8 Homocysteine

Deficiency of B vitamins (Folate, B6 and B12). Smoking Stress hostility will increase levels.

Homocysteine is an amino acid (a building block of protein) that is produced in the body. It can irritate blood vessels, leading to blockages in the arteries (atherosclerosis). High homocysteine levels in the blood can also cause cholesterol to change to a form that is more damaging to arteries (oxidized LDL low-density lipoprotein). In addition, high homocysteine levels can make blood clot more easily than it should, increasing the risk of blood vessel blockages. A blockage can cause a stroke or a problem with blood flow.

It is becoming apparent that too many people today have a homocysteine level that is higher than it needs to be. A high homocysteine level is found in up to 20% of people with heart disease.

Homocysteine is normally changed into other amino acids for use in the body's normal functions. If the level is too high, then you may not have enough B vitamins to help this natural process, or you may not have enough necessary chemicals (enzymes) to process homocysteine.

Most people with a high homocysteine level have a low dietary intake of folate (folic acid), vitamin B6 or vitamin B12. Replacement of these vitamins helps the homocysteine level return to normal. Other poss causes of an abnormally high homocysteine level include low thyroid hormone levels, kidney disease, psoriasis, some meds or inherited deficiencies in the enzymes used to process homocysteine in the body.

Homocysteine is measured through a simple blood test. It can be measured at any time of the day. It is not nec to prepare in any special way for the blood test (as fasting). Most hosp labs can measure homocysteine, or a blood sample can be sent out to a special lab.

A healthy homocysteine level is less than 12 mol per L. A higher level than 12 mmol per L is considered high. If your homocysteine level is 12-15 mol per L and you have blockages in any blood vessel, you need to lower your level to less than 12. If you have no other major risk factors for cardiovascular disease and you do not have atherosclerosis, it may be acceptable to have a modestly elevated level of homocysteine (12-15 mol per L).

While no studies have adequately determined whether lowering homocysteine levels will help to reduce strokes, heart attacks and other cardiovascular events, it is a good idea to lower your homocysteine level because of the known risk of heart disease with high levels of this amino acid. How can I lower a high homocysteine level?

Eating more fruits and vegetables (especially leafy green vegetables) can help lower your homocysteine level. Good sources of dietary folate include many breakfast cereals, lentils, chickpeas, asparagus, spinach and most beans. If adjustment of your diet is not enough to lower your homocysteine to a desirable level, you will also need to take specific vitamins. You may need to take a fairly large amount of folate (about 1 milligram per day). Additional vitamin B6 and vitamin B12 also help the body process homocysteine. Vitamin B supplements generally have no side effects.

If taking these additional supplementary vitamins does not lower your homocysteine level, your doctor may have you try higher vitamin doses, or you may need to have some tests to see if you inherited a condition that causes high homocysteine levels.

Taking high doses of vitamins is not generally recommended for heart disease prevention unless you have a high homocysteine level or some other metabolic abnormality. The usual recommended vitamin and folate doses for lowering homocysteine levels are as follows: A daily multivitamin containing 400 g of folate and less than 5 mEq of iron

An additional 800 g of folate per day for eight weeks It is important to get your homocysteine level rechecked after you have been taking the multivitamin and additional folate for eight weeks. If your homocysteine level remains high, your doctor will need to change your treatment. You may need to take more folate (2 mg per day). If you have had a high homocysteine level, you will probably need to have your level checked two or three times per year. If you have any questions about homocysteine and the treatment of your high homocysteine level, talk to your family doctor.

www.healthanswers.com

Between 1992 and 1996, 64 men and women in Norway quietly died. Their passing was noted by their families but otherwise was largely unremarked. All the deceased, after all, suffered from heart disease, and many had undergone bypass surgery. Deaths like these are not the stuff of headlines.

Last week, however, the dead Norwegians made the evening news. What all of them had in common, in addition to sickly hearts and premature deaths, was elevated levels of an amino acid called homocysteine. The patients were part of a study, published in the current issue of the New England Journal of Medicine, that shows an almost lockstep correlation between high homocysteine levels and coronary-disease mortality. And that paper follows more than 50 less publicized studies since 1992 suggesting similar connections.

What makes this research so compelling is that unlike cholesterol, which everyone knows is associated with coronary problems but can often be treated only by medication and a rigid diet, homocysteine appears to respond to nothing more demanding than eating more vegetables and taking a few more vitamins. Homocysteine is certainly not the lone gunman of heart disease, but the studies strongly suggest that it's at least a co-conspirator--and one that patients can do something about. "This is very convincing," says Dr. Jacob Selhub of Tufts University in Boston. "Homocysteine appears to be a risk factor for heart disease."

To a few doctors, homocysteine is nothing new. As long ago as 1969, Harvard physician Kilmer McCully--now with the Veterans Administration Hospital in Providence, R.I.--was studying the unusual case of an eight-year-old boy who had died of a stroke. McCully found that the boy's bloodstream was fairly awash in excess homocysteine and that his arteries had the sclerotic look of an elderly man's.

Ordinarily pretty harmless stuff, homocysteine is used by the body to help manufacture proteins and carry out cellular metabolism. Too much of it, however, appears to cause blood platelets to clump together and vascular walls to begin to break down. In older patients, a lifetime of this damage may give arteries the scarred and thickened texture that provides circulating cholesterol with a place to stick and grow. In the young boy, accelerated homocysteine production caused by a genetic defect apparently led to accelerated damage. In both instances, however, McCully points to the same chemical culprit. "The underlying cause of heart disease," he says, "is an imbalance in the system that controls homocysteine levels."

Superficially, at least, the New England Journal paper appears to confirm this. The study, conducted at Haukeland University Hospital in Bergen, Norway, surveyed 587 people with a history of heart trouble. The 64 who died during the course of the research were among those with the highest levels of homocysteine in their blood.

Overall, the research suggested, people with elevated homocysteine are 4 1/2 times as likely to die of heart disease as those with normal levels.

No one knows for certain what causes some individuals and not others to overproduce homocysteine. But the evidence points to a shortage of vitamin B6, vitamin B12 and folic acid, all of which work to convert the amino acid into a molecular form the body can use. The answer for people concerned about cardiac health would seem to be for them to keep their intake of the protective vitamins high. The Harvard Health Letter has recommended increasing consumption of a range of foods--including leafy green vegetables, beans, peas, grains and certain meats and dairy foods--to keep homocysteine in check. Many researchers agree. "Don't wait for the Messiah," says Selhub. "Start eating more vitamin-rich vegetables now. If you can't, take vitamin supplements."

Not everyone is sold on such a simple prescription. Even if homocysteine is behind some cases of heart disease, it's unlikely to be behind them all, and there's no guarantee that managing the amino acid will decrease the risk of cardiac trouble. Regardless of circulating homocysteine levels, smoking and obesity will still ravage the cardiovascular system, and a poor diet will still choke the blood with fats. Cardiologist Roger Blumenthal of Johns Hopkins University estimates the share of all cardiac cases attributable to homocysteine at fewer than 1 in 5.

What's more, even for patients whose illnesses are caused by elevated amino acids, diet may not be much of a cure. Scientists know cholesterol levels in the blood fluctuate within a limited range; when people eat less fat, the liver simply manufactures more.

It's not yet known whether there is a similar set point for homocysteine. "People are jumping the gun if they think they can just take vitamins and skip the traditional health measures like exercising and eating a low-fat diet," says Blumenthal. "All the evidence has yet to come in." Nonetheless, in a field of medicine in which the bad news often surpasses the good, the evidence that came in last week was encouraging indeed.

HOW THE DAMAGE IS DONE 1 Protein-rich foods contain an amino acid, methionine, that converts to homocysteine 2 Excess levels of homocysteine damage the lining of arteries 3 Cholesterol builds up inside the scarred arteries, which can lead to fatal blockages

THE BEST DEFENSE Vitamins found in fresh foods and in supplements break homocysteine down VITAMIN B12 Found in such foods as meat, fish and dairy products VITAMIN B6 Found in green leafy vegetables, pultry, nuts, whole-grain cereals, fish FOLIC ACID Found in green leafy vegetables, fruits, orange juice, wheat germ, dried beans, peas When taken in daily supplements, 100 micrograms of B12, 10 mg of B6 and 1 mg of folic acid is recommended Source: Dr. Kilmer McCully, The Homocysteine Revolution

By JEFFREY KLUGER REPORTED BY DAVID BJERKLIE/NEW YORK

In 1968, Kilmer McCully, a researcher at Harvard University Cambridge, Mass., proposed a link between elevated blood levels of homocysteine (a breakdown product of protein metabolism) and the development of coronary heart disease. Few took his theory seriously then, but today, the impact of his discovery finally is being appreciated. Elevated homocysteine, which can be caused by inadequate intakes of the B vitamin folic acid, is recognized as an important risk factor for heart disease.

According to McCully, now a staff pathologist at the Providence (R.I.) Veterans Administration Medical Center, numerous studies have confirmed his finding that elevated homocysteine is an independent risk factor for arteriosclerosis, heart attack, stroke, and vascular disease. In the Framingham (Mass.) Study, which has been monitoring causes of heart disease for more than 50 years, there was a strong correlation between blood levels of homocysteine and occurrence of stenosis (narrowing of the arteries due to plaque buildup). Stenosis appeared in 58% of men with the highest levels of homocysteine, compared with 27% in the lowest levels. Approximately two-thirds of all cases of elevated homocysteine were associated with inadequate intakes of one or more of B[sub 6], B[sub 12], and folate.

The sole source of homocysteine in the body is the amino acid methionine, which comes from dietary proteins. During normal metabolism, methionine continually is converted to homocysteine and back to methionine. Vitamins B[sub 6], B[sub 12], and folic acid are essential for these conversions to occur. Without proper metabolism, the buildup of homocysteine--homocysteinemia--eventually can cause damage to the blood vessels. In addition to dietary inadequacies, other factors that can cause homocysteinemia include certain drugs, hormones, and aging. Genetics also may play a major role.

Rima Rozen, associate professor of genetics, human biology, and pediatrics at Canada's McGill University-Montreal Children's Hospital, has investigated the role of folic acid derivatives in several different metabolic pathways, such as DNA synthesis and homocysteine conversion to methionine. She found mutations in the gene responsible for making the enzyme necessary to synthesize the active form of folic acid. "We estimate that 10-12% of the North American population carries two mutant copies of this gene and is at risk for developing high plasma homocysteine if they don't have enough folic acid to compensate. Individuals with this mutation may have higher requirements for folic acid to prevent buildup of homocysteine levels. Once identified, these individuals may significantly lower their risk for heart disease by taking folic acid."

The altered metabolism results in an imbalance where levels of methionine are in excess and those of B vitamins are insufficient. Consequently, a form of homocysteine that is related to formation of lipid plaques in blood vessels is allowed to form and reach elevated, harmful levels. In most cases of elevated homocysteine, B vitamin supplements are the first line of defense.

What's "normal"? That's the question dozens of researchers and some physicians are now asking themselves about homocysteine, a substance in blood that may rival cholesterol as a major actor in the nation's leading killer, heart disease, and play an important role in other common health problems as well.

Recent evidence has implicated elevated blood levels of homocysteine, an unhappy byproduct of normal metabolism, in conditions ranging from miscarriages and birth defects to strokes, Alzheimer's disease and other disorders that afflict older people, including osteoporosis and presbyopia, the eye changes that force the middle-aged to acquire reading glasses.

And since hostility and stress raise blood levels of homocysteine, it may explain why these emotional states are linked to heart attacks. Though strong hints of homocysteine's ability to damage arteries date back more than 30 years, until the 1990's its importance in cardiovascular disease was completely overshadowed by cholesterol.

While concerns about elevated cholesterol levels fingered dietary fat as the culprit, high levels of homocysteine are associated with a diet rich in animal protein, the source of homocysteine's parent compound, the amino acid methionine.

Furthermore, as Dr. Meir Stampfer of the Harvard School of Public Health pointed out, "there was no commercial interest in studying homocysteine," since the way to reduce it -- eating less meat and taking supplements of B vitamins -- is inexpensive and not patentable. For cholesterol, on the other hand, pharmaceutical companies seeking to sell cholesterol-lowering drugs paid for many studies.

In addition, homocysteine's potential role in common disorders may have been overlooked because the levels associated with an increased risk of health problems are still listed as normal by medical laboratories -- 8 to 20 micromoles per liter of blood plasma. However, recent studies have linked levels as low as 15 micromoles to an increased risk of heart attack, stroke, peripheral vascular disease and venous thromboembolism, potentially life-threatening blood clots in the veins.

Among the 15,000 doctors participating in the Physicians' Health Study, those with a homocysteine level of 15 micromoles or higher had a heart attack rate three times as high as those with lower levels over a period of just five years, Dr. Stampfer and his Harvard colleagues found. Even a level of 12 micromoles can double coronary risk. Dr. William Castelli, former director of the Framingham Heart Study, who now heads the Framingham Cardiovascular Institute in Massachusetts, considers levels higher than 9 micromoles to be elevated, placing people at increased risk of a heart attack or stroke. In the Framingham study, he said, about 40 percent of the people had homocysteine levels greater than 9.

"Homocysteine is an important new risk factor for cardiovascular disease," Dr. Castelli said in an interview. "There are about 17 studies now under way to determine the benefits of lowering homocysteine levels. We're still missing crucial data. We don't yet know if lowering homocysteine will result in a lower rate of heart attacks or strokes." The studies are being financed by the National Institutes of Health.

But Dr. Castelli and others pointed out that since the way to bring down homocysteine -- eating less meat and taking supplements of the B vitamins folate, B6 and B12 that are required by the enzymes that process homocysteine -- is harmless and inexpensive, people should not have to wait five or more years for the research results before trying to lower their own homocysteine levels.

There are several ways in which homocysteine can damage blood vessels. It injures the cells that line arteries and stimulates the growth of smooth muscle cells; both effects can result in lesions that narrow the channels through which blood flows. Homocysteine can also disrupt normal blood clotting mechanisms, increasing the risk of clots that can bring on a heart attack or stroke.

Damage to the small blood vessels in the brain may explain the relationship that has been found between elevated homocysteine levels and the loss of cognitive function and Alzheimer's disease, say Dr. Jacob Selhub and colleagues at the United States Department of Agriculture Human Nutrition Research Center on Aging at Tufts University in Boston. Starting in 1983, they noted, several studies have linked an inadequate supply of B vitamins to a decline in cognitive function in the elderly, and some studies have shown that taking supplements of B vitamins improves cognitive performance.

For example, this year in the American Journal of Clinical Nutrition, Dr. David A. Snowdon and colleagues at the University of Kentucky College of Medicine in Lexington described a study of 30 nuns who had lived in the same convent and eaten from the same kitchen until their deaths at ages 78 to 101. Blood samples taken years earlier revealed that those who had low blood levels of the B vitamin folate were far more likely to have suffered atrophy of the cerebral cortex. The lower the folate levels, the more severe the atrophy of the nuns' brains.

As for other disorders common in the elderly, Dr. Carlos L. Krumdieck and Dr. Charles W. Prince, nutrition scientists at the University of Alabama Schools of Medicine, Dentistry and Health Related Professions in Birmingham, have described a link between moderately elevated homocysteine levels and the occurrence of senile osteoporosis and presbyopia. They pointed out that the contribution of chronically elevated homocysteine levels "to diseases of old age may have gone unrecognized because we are conditioned to accept them as inescapable consequences of growing old."

The harmful effects of homocysteine on blood vessels and blood clotting may also explain the link between elevated levels of this amino acid and various pregnancy complications, including repeated early miscarriage; pre-eclampsia, or pregnancy-related hypertension; premature birth; very low birth weight; and certain birth defects. Researchers at the University Hospital Nijmegen St. Radboud in the Netherlands reported recently in the journal Obstetrics and Gynecology that 123 women who had experienced repeated early miscarriages had "significantly lower serum folate concentrations" and higher levels of homocysteine than a comparison group of 101 women who had not had miscarriages.

In another recent report in the American Journal of Clinical Nutrition, researchers in Bergen, Norway, found that among 5,883 women who had a total of 14,492 pregnancies, those with the highest levels of homocysteine were significantly more likely to have experienced pregnancy complications like pre-eclampsia, premature birth and very low birth weight than women with the lowest homocysteine levels.

It has been known for some time that increasing a woman's intake of folate during the first three weeks of pregnancy can greatly decrease the risk of often lethal spinal deformities like spina bifida and anencephaly in the fetus. This prompted the Food and Drug Administration to order, as of January 1998, fortification of all flour and grain products with folate, a measure that Dr. Selhub said had reduced elevated homocysteine levels in the general population by about 10 percent. Although a practicing physician reviewing a patient's laboratory test report may understandably dismiss a homocysteine level of, say, 12 micromoles as normal, a 1995 analysis of 27 studies indicated that there was no absolute safe blood level of this substance. Rather, as with cholesterol, the risk associated with homocysteine is on a continuum; an increase of only 5 micromoles in the plasma level of homocysteine can raise a person's chances of developing cardiovascular disease by as much as a 20-milligram rise in cholesterol would. Other reports have equated homocysteine's risk to the cardiovascular system with the damage done by smoking or a high blood level of cholesterol.

In fact, the emerging appreciation of the risks associated with so-called normal levels of homocysteine parallels the experience with cholesterol. As recently as two decades ago, doctors regarded cholesterol levels in blood plasma of 240 milligrams as normal, but now levels above 200 milligrams are recognized as increasing a person's risk of developing cardiovascular disease. And, as with cholesterol, homocysteine levels tend to rise with age and are generally higher in men than in women, at least until women reach menopause.

Homocysteine also appears to exacerbate the effects of other cardiovascular risks. For example, high homocysteine "substantially increases the risk associated with smoking and hypertension," Dr. Iftikhar J. Kullo and colleagues at the Mayo Clinic pointed out. And among people with diabetes, a recent study from the Netherlands found that for each five-micromole rise in homocysteine, the risk of dying from any cause over a five-year period was more than triple that of nondiabetics with the same homocysteine levels.

Homocysteine is an amino acid, an intermediate product that builds up when the amino acid methionine cannot be converted to cysteine because an enzyme is lacking or is present in inadequate amounts. The B vitamins folic acid, or folate, and B6 and B12 are crucial to these conversion enzymes. But it has not yet been demonstrated that taking vitamins to lower homocysteine will prevent heart disease or any other disorder linked to homocysteine.

What is known so far is that vitamin therapy can slow and even reverse clogging of the carotid arteries that feed the brain, which should reduce the risk of stroke. Dr Daniel G. Hackam and colleagues at the Siebens-Drake/ Robarts Research Inst in London, Ont, showed a reversal of carotid artery clogging in patients with homocysteine levels both above and below 14 micromoles who took 2.5 milligrams of folic acid, 25 milligrams of B6 and 250 micrograms of B12 daily for a year.

They concluded that "these observations support a causal relationship between homocysteine and atherosclerosis and, taken with epidemiological evidence, suggest that in patients with vascular disease, the level to treat may be less than 9 micromoles per liter."

The homocysteine story actually began in 1969 when Dr Kilmer S. McCully reported that children born with a genetic error of metabolism that causes their homocyst-eine levels to skyrocket to hundreds of micromoles died with advanced disease in their arteries at a very young age.

In the last two decades there were occasional reports of advanced clotting in arteries feeding the brains of children with homocystinuria, as the genetic condition is called. In other cases, seriously thickened walls of the carotid arteries were found in young adults born with only one of the two genes that cause homocystinuria.

But, perhaps because in most people homocysteine levels rarely exceed 30 micromoles, until recently few resear-chers appreciated the significance of Dr McCully's finding or any of the subsequent observations in people with homocysteine levels in the hundreds of micromoles.

Meanwhile, Dr McCully lost his research financing and his job at Mass Gen Hosp and Harvard Med School and was forced to do what little he could to pursue the homo-cysteine hypothesis on his own while working at the VA Med Ctr in Providence, RI.

Dr McCully, who is now enjoying renewed respect with the emergence of homocysteine as a cardiovascular risk factor, considers arteriosclerosis, a clogging of the arteries with fats and other substances, to be a disease of "protein intoxication." While Americans are busy focusing on fat avoidance to lower cholesterol, he believes they should be reducing their consumption of animal protein to lower homocysteine.

Indeed, a study recently published in Preventive Med by Dr. David J. DeRose of the Lifestyle Center of Amer in Sulphur, Okla., and colleagues showed that a diet devoid of animal products, caffeine and alcohol, along with exercise, stress mgmnt and spiritual support - but no B vitamin supplements - reduced homocysteine levels in 40 men and women by an aver of 13% in just one week.

"I'm thrilled that scientists all over the world are now taking up the question of homocysteine and heart disease" Dr McCully said. "An avalanche of studies has demonstr-ated the validity of this approach, and I anticipate that the studies now underway will prove that controlling homocysteine is the best way to deal with heart disease."

What is homocysteine, and how is a high homocysteine level harmful? Homocysteine is an amino acid (a building block of protein) that is produced in the human body. Homocysteine may irritate blood vessels, leading to blockages in the arteries (called atherosclerosis). High homocysteine levels in the blood can also cause cholesterol to change to a form that is more damaging to arteries (called oxidized low-density lipoprotein). In addition, high homocysteine levels can make blood clot more easily than it should, increasing the risk of blood vessel blockages. A blockage might cause you to have a stroke or a problem with blood flow.

What causes a high homocysteine level? It is becoming apparent that too many people today have a homocysteine level that is higher than it needs to be. A high homocysteine level is found in up to 20 percent of people with heart disease.

Homocysteine is normally changed into other amino acids for use in the body's normal functions. If your homocysteine level is too high, then you may not have enough B vitamins to help this natural process, or you may not have enough necessary chemicals (enzymes) to process homocysteine.

Most people with a high homocysteine level have a low dietary intake of folate (also called folic acid), vitamin B6 or vitamin B12. Replacement of these vitamins helps the homocysteine level return to normal. Other possible causes of an abnormally high homocysteine level include low thyroid hormone levels, kidney disease, psoriasis, some medications or inherited deficiencies in the enzymes used to process homocysteine in the body.

How is the homocysteine level measured, and what do the results mean? Homocysteine is measured through a simple blood test. It can be measured at any time of the day. It is not necessary to prepare in any special way for the blood test (such as fasting). Most hospital laboratories can measure homocysteine, or a blood sample can be sent out to a special laboratory.

A healthy homocysteine level is less than 12 mol per L. A level of greater than 12 mmol per L is considered high. If your homocysteine level is 12 to 15 mol per L and you have blockages in any blood vessel, you need to lower your homocysteine to less than 12 mol per L. If you have no other major risk factors for cardiovascular disease and you do not have atherosclerosis, it may be acceptable for you to have a modestly elevated level of homocysteine (12 to 15 mol per L).

While no studies have adequately determined whether lowering homocysteine levels will help to reduce strokes, heart attacks and other cardiovascular events, it is a good idea to lower your homocysteine level because of the known risk of heart disease with high levels of this amino acid. How can I lower a high homocysteine level?

Eating more fruits and vegetables (especially leafy green vegetables) can help lower your homocysteine level. Good sources of dietary folate include many breakfast cereals, lentils, chickpeas, asparagus, spinach and most beans. If adjustment of your diet is not enough to lower your homocysteine to a desirable level, you will also need to take specific vitamins. You may need to take a fairly large amount of folate (about 1 milligram per day). Additional vitamin B6 and vitamin B12 also help the body process homocysteine. Vitamin B supplements generally have no side effects.

If taking these additional supplementary vitamins does not lower your homocysteine level, your doctor may have you try higher vitamin doses, or you may need to have some tests to see if you inherited a condition that causes high homocysteine levels.

Taking high doses of vitamins is not generally recommended for heart disease prevention unless you have a high homocysteine level or some other metabolic abnormality. The usual recommended vitamin and folate doses for lowering homocysteine levels are as follows: A daily multivitamin containing 400 g of folate and less than 5 mEq of iron

An additional 800 g of folate per day for eight weeks It is important to get your homocysteine level rechecked after you have been taking the multivitamin and additional folate for eight weeks. If your homocysteine level remains high, your doctor will need to change your treatment. You may need to take more folate (2 mg per day). If you have had a high homocysteine level, you will probably need to have your level checked two or three times per year. If you have any questions about homocysteine and the treatment of your high homocysteine level, talk to your family doctor.

www.healthanswers.com

On Whether to Have Your Homocysteine Level Measured ? Tufts Univ Health and Nutrition Letter. March 1998 Evidence is mounting that some people at risk for coronary disease should be tested and treated for elevated blood levels of a substance called homocysteine (ho-mo-SIS-teen). We all have homocysteine in our blood; it is a breakdown product of an amino acid found in protein-containing foods.

In healthy people, homocysteine levels are kept in check by three B vitamins: folate, B6, and B12. But when those vitamins are in short supply in the body, excess homocysteine accumulates. High concentrations of homocysteine are thought to make the artery walls sticky, allowing blood cholesterol to build up and block the flow of blood through the body. No doubt that's why studies throughout the world are finding a link between elevated homocysteine and heart disease. Some research suggests that as many as 15 to 30 percent of all patients with blocked arteries have too much homocysteine in their blood.

High homocysteine can be detected by blood tests, which might make it sound as though it should be checked for as routinely as high blood cholesterol. "But testing is not something that can be recommended on a widespread basis," says Ronald Krauss, MD, Chairman of the American Heart Association Nutrition Committee. Despite the inroads scientists have made concerning homocysteine's effect on heart disease, relatively little is still known about the connection, so testing for everyone would be premature at this time. It has not been proven, for instance, that lowering homocysteine levels in the blood automatically reduces heart attack risk. In addition, testing can be inconvenient and expensive -- your doctor may have to send your blood to a lab that is specially equipped to measure homocysteine.

Despite the caveats, testing makes sense for people who already have heart disease or a strong family history of premature heart disease, says Paul Jacques, ScD, acting Chief of epidemiology at the Human Nutrition Research Center at Tufts. Learning one's homocysteine level and lowering it if it's high is a way for someone at high risk to hedge his or her bets before all the facts are in.

Researchers differ on exactly what constitutes optimal and high levels of homocysteine. Some say optimal is 12 micromoles (per liter of blood) or less; borderline is 12 to 15; and high risk is 16 and above. Others consider a reading over 12 to be high. "We're still in the dark ages" regarding homocysteine numbers, Dr. Jacques says. "But it's safe to say that levels over 16 would be classified as high."

B Vitamins to the Rescue The good news is that in most cases, elevated levels of homocysteine in the blood can be reduced with folate and vitamins B6 and B12. As far as the amounts to consume, "it hasn't been tested very well," says Ernst Schaefer, MD, a heart disease researcher at Tufts.

Thus, recommendations differ. But Dr Schaefer, along with others, suggests that people with heart disease take a daily multivitamin supplement that contains 400 micro-grams of folate; 4 milligrams of B6; and 8 micrograms of B12. People without heart disease should also aim for 400 micrograms of folate. But 3 milligrams of B6 are probably enough, as are 6 micrograms of B12.

Where the Bs Are - In a new study that looked at the eating habits of some 80,000 women, research at Harvard found that those who took in at least 400 micrograms of folate a day and 3 milligrams of B6 were significantly less likely to suffer heart attacks than those who had much lower levels. Foll are sources of those vitamins along with sources of B12, also thought to lower homocys-teine levels and thereby reduce heart disease risk.

micrograms of folate (aim for 400 a day) 1/2 cup lentils 179 1/2 cup chickpeas 141 1/2 cup kidney beans 115 1/2 cup frozen spinach 102 1 cup General Mills Cheerios 100 1 cup Kellogg's Corn Flakes 100 1 cup Ronzoni spaghetti 100 6 oz orange juice (from frozen conc.) 82 1/2 cup frozen Brussels sprouts 79 1/2 cup frozen chopped broccoli 52 1 baked potato with skin 0.7 1 banana 0.7 1 cup Post Raisin Bran 0.7 3 oz roasted light-meat chicken 0.5 3 oz beef tenderloin 0.4 1/2 cup mashed sweet potato 0.4 1/2 Florida avocado 0.4 3 oz lean roasted pork 0.4 3 oz tune canned in water 0.3 6 oz canned vegetable juice cocktail 0.3 1 1/3 cups General Mills Total 6.0(***) 3 oz tune canned in water 2.5 3 oz beef tenderloin 2.2 2 Atlantic sardines 2.0 3 frozen fish sticks 1.5 1 cup yogurt 1.0 1 cup skim milk 0.9 3 oz broiled pork loin 0.9 1.6-oz beef frankfurter 0.7 1 oz Swiss cheese 0.5 3 oz roasted light-meat chicken 0.3 1/2 cup Minute Rice 40 1 ear of corn 0.2 micrograms of B12*

*For foods that require cooking, values are for cooked weighted or volume. **People who have heart disease will probably need a multivitamin supplement that contains B vitamins to meet the higher goal. ***B12 is found naturally only in foods of animal origin, although a nbr of bfst cereals are fortified with it.

\9 Urinary incontinence

 is an uncontrollable loss of urine. About 10 million American adults have problems with incontinence, with about 50% of women reporting occasional urine loss. It affects millions of people. Its complications are annoying and embarrassing and can force major lifestyle changes.

There are two primary types of incontinence.Urge incontinence is urinary leakage that comes from a sudden, uncontrollable urge to urinate. It is more common in the elderly, both women and men, and is tied to a degenerative process in the central nervous system affecting the bladder. Urge incontinence also can be caused by tumors or by neurologic diseases such as Parkinson's or multiple sclerosis.

Treatments range from medications to biofeedback, hormone therapy, behavior modification and a variety of surgical procedures. But before the appropriate treatment can be chosen, patients must be evaluated thoroughly to determine the cause of their incontinence, detect associated vaginal wall prolapses and assess the impact of incontinence and/or prolapses on their lives.

Evaluation includes a comprehensive medical history, a physical examination, laboratory analysis of urine and blood, and - when indicated - diagnostic imaging by X-ray or fluoroscopy and bladder testing.

Incontinence affects 10 million to 20 million women, mostly between the ages of 40 and 60. Stress incontinence is the most common form among women under 65 and can be caused by weakening of the vaginal wall that supports the urethra. It also can be the result of a sphincter that isn't working properly. Women with incontinence have to contend with urinary leakage when they move briskly, change position suddenly, cough or sneeze. Since they never know exactly when or where it is going to happen, many wear a pad - a diaper for adults.

That's a difficult and embarrassing existence. But researchers at UT Southwestern Medical Center at Dallas say women with incontinence can be treated effectively.

Incontinence can be caused by changes of the vaginal wall which can be weakened by pregnancies and deliveries, hormonal changes, pelvic surgery or aging. Incontinence in women also can be associated with other areas of vaginal wall relaxation, resulting in bladder drop, known as prolapse, or bulge of the rectum through the vaginal wall. A defective sphincter caused by surgeries, injury, pelvic radiation or nerve disorders also can be at fault.

Effective incontinence treatment is possible and your physician can help develop a plan that will work for you.

Incontinence Treatment A new high-tech treatment may help solve the embarrassing problem of incontinence for some patients. The Sacral Nerve Stimulation System, a new treatment for incontinence, recently became approved for general clinical use in the US. This device works a lot like a heart pacemaker. It stimulates the sacral nerve, helping patients control their bladders.

Doctors at UT SW Med Center at Dallas say this device is best suited for patients whose incontinence has disrupted their lives but who haven't seen improvement from other incontinence treatments, like dietary changes, medication and biofeedback. For these patients, leaving home can be traumatic because they always have to know where the nearest bathroom is, and they can seldom enjoy activities like going out to dinner or to a movie.

To be considered for the nerve stimulation system, patients must undergo testing. Their kidneys and ureters must function normally, and their bladders must be capable of holding a normal amount of urine. Patients also must respond well to tests stimulating the sacral nerve. More than half the patients in clinical trials reported that their symptoms improved by 90 percent with the nerve stimulation.

Responses vary by individual, and it may take up to six months to notice an improvement. There are only a few places in the country that currently offer this treatment. Talk to your doctor to see if it's right for you and to find a place where you can be treated.

 Holding It In If you're afraid to laugh in public, or if you're keeping an eye out for the nearest restroom, it may be time for a trip to the doctor.

Millions of older women are embarrassed to laugh in public. That's because they suffer from a condition called stress incontinence. When they laugh or cough, a little bit of urine leaks. It's a common problem that comes with age, when muscles and nerves in the bladder may weaken or change. Doctors at UT Southwestern Medical Center at Dallas say you shouldn't suffer from this problem in silence. Talk to your doctor. Treatments are available. Exercises to strengthen the muscles that control your bladder may help, and in some severe cases, surgery may resolve the problem.

Other people suffer from an overactive bladder, which causes a frequent need to urinate. People with this condition are afraid to get too far from a bathroom. This is another reason to see your doctor. UT Southwestern urologists say the first step is a urinalysis because one of the most common causes of overactive bladder is a urinary-tract infection. Other potential causes include tumors or stones within the urinary tract. These are possibly serious and need to be checked.

Sometimes it's embarrassing to talk to your doctor about something so personal, but getting the right treatment can improve your quality of life -- and in some cases, may even save your life. Your doctor will understand your discomfort and will work with you to find the right solution.

 Urinary incontinence takes several distinct forms: Stress incontinence, the most common type, is an involuntary loss of urine during coughing, straining, sneezing, lifting, exercising, or any other activity that increases pressure within the abdomen. Urge incontinence is a sudden loss of urine, sometimes in large amounts, just after feeling a strong, unexpected urge to urinate. Overflow incontinence is leakage of small amounts of urine from a full bladder. A person with this type of urine loss can no longer feel the sensation of a full bladder and never empties it completely, so urine often "spills out." Total incontinence results when the urinary sphincter doesnt fully close, so urine constantly drips out. Some people are born with this problem, in others it is the result of an injury to the "neck" of the bladder, where the sphincter is located. Functional, psychological, or environmental incontinence is a loss of urine in a person who, for whatever reason, cannot get to the toilet or get a bedpan when needed. The urinary system might work well, but other problems keep the person from using the bathroom in the usual way. Mixed incontinence is a combination of types. Older women, for example, often have both stress and urge incontinence.

Urinary tract infection, vaginal infection or irritation, constipation, obesity, smoking, high-impact aerobics, and side effects of drugs can all trigger temporary or recurrent urinary incontinence. Causes of long-terms problems with urine loss include the following:

aging (not inevitable with aging, but the aging bladder tends to hold less urine and the urine stream can get weak, leading to overflow problems) weakness of the bladder and the muscles that support the urinary tract weak pelvic muscles due to pregnancy and long, difficult vaginal births overactive bladder muscles a blocked urethra (often caused by prostate enlargement in men) hormone imbalances in women neurological disorders a prolapsed uterus structural abnormalities of the urethra injuries to the urinary tract bladder stones and tumors emotional or mental problems, such as depression diabetes mellitus

Women are far more prone to urine loss than are men for several reasons. Childbirth takes a heavy toll on the bladder and the sphincter muscle that controls urine flow. Also, low levels of female hormones during and after menopause thin and weaken the tissues of the urinary tract, leading to urine loss.

DETECTION AND DIAGNOSIS To diagnose the type of incontinence involved and to plan the right treatment, the doctor will take a thorough medical history, including urinary habits. In women, a vaginal examination reveals any physical causes, such as a cystocele (dropped bladder) or a prolapsed uterus, as well as thinning tissues due to depleted hormones. A rectal exam helps the doctor evaluate sphincter and muscle tone, and in men, the size of the prostate.

The doctor might also request blood and urine tests, as well as a cystoscopic examination, during which the doctor views the inside of the bladder and the lower urinary tract by inserting a small tube with a telescope attached. Inserting a small, soft tube into the bladder after the patient urinates can tell the doctor how much urine is left in the bladder (called residual urine). The doctor can also test for stress incontinence by asking the patient to cough or strain. Urodynamic testing, another diagnostic aid, involves passing water into the bladder through a small, flexible tube. The pressures inside the bladder at various stages of fullness are recorded, and those patterns of pressure help the doctor diagnose the type of problem and plan treatment.

TREATMENT cures about 70% of cases, or at least improves. Left untreated, it is likely to get worse. Treatment for most types of incontinence begins with eliminating bladder irritants, such as caffeine-based and carbonated beverages, citrus fruits and juices, chocolate, highly spicy foods, and alcohol. The doctor will also advise a healthful, balanced diet; a regular program of sensible exercise; and weight loss if the patient needs it. And of course, any underlying med conditions causing the problem must be treated.

For stress incontinence, many options are avail, starting with pelvic muscle rehabilitation. This includes pelvic muscle exercises, biofeedback therapy, vaginal weight training, and pelvic floor electrical stimulationall done to strengthen the muscles around the vagina and the urethra. Pelvic muscle exercises, called Kegel exercises, involve contracting the muscles of the urethra, vagina, and rectum for a set period of time, and then relaxing them. To learn the technique, a woman slowly contracts these muscles while urinating, then holds the position for 10 seconds before releasing. Proper contraction will stop the flow of urine. The exercise is repeated several times and can be done in other positions and at other times. For women who have trouble doing it correctly, biofeedback training can help. With several electrodes in place on the womens abdomen and a probe inserted in the vagina, a monitor displays the force of her muscle contractions. That way, she can tell if she is using the right muscles and if she is squeezing hard enough. She can also practice controlling the urge to urinate as the bladder fills. With vaginal weight training, a woman inserts progressively larger cone-shaped vaginal weights into her vagina, pointed end down, and practices keeping them in place twice a day. Once a weight can be retained for 20 to 30 minutes, it is time to progress to the next size weight. Over several weeks, the pelvic muscles become toned and conditioned until they are again operating at full strength. With bladder retraining, patients learn to "hold on" for increasing amounts of time, and to urinate at regular, scheduled intervals. This method teaches patients to resist the urge to urinate and to lengthen the intervals between urination. With pelvic floor electrical stimulation, a battery-operated electrode placed in the vagina or rectum delivers mild impulses that trigger muscle contractions. Over time, this helps strengthen the pelvic muscles.

Stress incontinence can also be treated with drugs that tone the urinary sphincter, such as ephedrine, pseudoephedrine, and phenylpropanolamine. Postmenopausal women who have urine loss due to the thinning or drying of urethral walls might benefit from applying a vaginal estrogen cream. Collagen injections around the urethra are another option. The strategically placed collagen adds bulk to the tissues of the urethra, thus closing the gap that allowed urine to leak. Some women benefit from inserting special devices called pessaries into the vagina to help support the pelvic muscles. Others use a single-use, tampon-like product called the Reliance Urinary Control Insert, available by prescription only. The woman uses a special applicator to insert the device into the urinary channel. A gentle push on the applicator inflates a small balloon that acts as a barrier to prevent urinary leakage. Reliance can be worn for up to six hours or until the woman wants to urinate. She then pulls a string to deflate the balloon, discards the device, and replaces it with another after urination.

Although considered an option only for those with severe stress incontinence, surgery has about a 90% cure rate. A wide variety of procedures are available, including creating a vaginal "sling" to support the urethra, implanting an artificial sphincter (a device that can be inflated to block urine flow), and repairing the bladder neck.

Urge incontinence is treated with bladder retraining, drugs that relax the bladder, such as propantheline or imipramine, or surgery to stabilize or reposition the bladder neck. Overflow incontinence is usually treated surgically or with drugs that relax the bladder, such as terazosin. Total incontinence is usually treated surgically. Functional, psychological, and environmental incontinence is treated with drugs, bladder retraining, or help using or getting to the toilet, depending on the cause. Mixed incontinence is treated with any of the above, depending on the causes and types involved.

PREVENTION measures might help prevent urinary urine loss: exercising regularly, including Kegel exercises for women who have undergone childbirth taking hormone replacements (postmenopausal women) urinating when the need arises instead of "holding it" (not to be confused with bladder retraining once incontinence has set in)

 For the last decade, Susan, a Long Island businesswoman who recently turned 50, has been plagued by an annoying and potentially humiliating problem: She has to empty her bladder a dozen or more times a day and several times a night, or risk an embarrassing accident. When she has to go, she has to go, and soon. Fortunately, Susan is not shy about seeking out lavatories wherever she may be.

But for more than 17 million Americans who share her problem of an overactive bladder, opportunities to urinate at a moment's notice are often limited, forcing them to restrict their activities, including their employment, to places and circumstances where loo are immediately avail. Some become homebound, going out only when they can be certain of quick access to a loo. Many are forced to wear adult diapers, dressing in loose clothes to hide the bulge and tell-tale signs of an occasional accident.

Sleep is often disturbed by the need to urinate often during the night, resulting in daytime fatigue that can impair work and social activities. Sexual activity may be avoided for fear of an embarrassing loss of bladder Ctrl.

The problem is far more challenging than the more common condition of stress incontinence, where a small amount of urine can escape when a sneeze, cough, hearty laugh or vigorous exercise puts pressure on the bladder. When a person with an overactive bladder loses control, the entire bladder is likely to empty at once. And while stress incontinence is primarily a problem for women, especially as they age, overactive bladder afflicts men and women in nearly equal numbers, and can occur at any age.

Although an overactive bladder is hardly rare and often has costly emotional, social and occupational consequences, most people with the condition accept it as a normal part of aging, which it is not, and sometimes are too embarrassed to tell even their doctors about it. Others remain silent because they believe -- or have been told -- that nothing can be done to control the problem. And yet, treatments, including a recently approved drug with relatively few side effects, are available that can significantly reduce if not eliminate the distress, discomfort and inconvenience associated with an overactive bladder. The bladder has an elastic wall containing a smooth muscle, the detrusor muscle, which in adults can tolerate a large increase in urine before a signal is sent to the brain that the bladder is about three-fourths full and needs to be emptied. Until that time, signals from the brain suppress contractions of the detrusor muscle, and thus inhibit emptying of the bladder. People with normal bladder function usually register a need to void at a bladder volume of about 250 milliliters, or about 8 ounces, of urine. If voiding is not convenient at that point, it can usually be delayed through voluntary control until the volume of urine is about double that amount. However, an overactive bladder in an adult behaves somewhat like the normal bladder of babies and young children, whose brains cannot yet control the time and place of voiding. In those with an overactive bladder, a sense of urgency typically occurs at a urine volume of about 150 milliliters. Inhibitory signals from the brain fail to suppress the overactive detrusor muscle and it contracts inappropriately during the bladder-filling phase, causing involuntary voiding. People with overactive bladders experience at least two of three major symptoms: a need to empty the bladder more than eight times in 24 hours, sometimes soon after they have done so; sudden sensations of urgency, and urge incontinence -- a leakage of urine or total bladder emptying if the urge is very strong or the person cannot reach the toilet quickly. In most cases, the underlying cause is unknown. However, overactive bladder sometimes results from certain neurological disorders, including multiple sclerosis, stroke, Parkinson's disease, spina bifida and spinal cord damage.

Most important in arriving at a correct diagnosis of an overactive bladder is obtaining a thorough history of urinary symptoms and eliminating other possible causes. The most common is a urinary tract infection, typically determined by a urine culture and often by the presence of blood in the urine. The doctor should also perform an abdominal and pelvic examination, looking for such anomalies as tumors, an enlarged prostate gland, a dropped uterus or other abnormal sources of pressure on the bladder or urinary tract. A doctor may also ask the patient to keep a daily chart of urinary output to determine whether the bladder empties fully during voiding since there may be an obstruction or inadequacy of the detrusor muscle resulting in poor bladder emptying. Sometimes a doctor will need to directly record bladder pressure during filling and voiding, a measurement known as cystometry. In an overactive bladder, peaks of increased pressure by the detrusor muscle are recorded during the filling phase, indicating periods of involuntary muscle contraction at a time when a normal muscle remains relaxed. There are two main approaches to treatment: bladder training and drug therapy. Bladder training aims to restore bladder control by increasing the capacity of the bladder before it registers the urge to void. The patient keeps a record of the frequency and volume of output, gradually increasing the time between voidings by 15 minutes until an interval of two to four hours is reached without leakage. A doctor may also ask a patient to keep a record of fluid intake, in case excessive fluids are contributing to the problem. However, most patients with overactive bladders have already cut back on the amount of fluids they consume, and some actually become seriously dehydrated. Bladder training is very demanding and must be maintained indefinitely to remain effective. For those reason, patients much prefer drug treatment. However, until this year, the available drugs brought side effects like dry mouth, constipation, blurred vision, confusion and urinary retention that prompted most patients to stop taking them. Drugs that are effective against overactive bladder are known as antimuscarinic agents because they hook up with muscarine receptors in the bladder and other organs throughout the body. The newest such drug, tolterodine, has a stronger attraction for the receptors in the bladder than those in other organs. Thus, bothersome side effects are much reduced and patients are more likely to continue therapy.

Bettye Roussos, a 57-year-old saleswoman from Ormand Beach, Fla., says the drug, under the trade name Detrol, has given her back her life. She once had a voiding accident while on a podium to receive an award. She regularly soaked through large protective pads. She feared going anywhere that was more than an hour's drive, and she began emptying her bladder hourly in the hope of avoiding accidents. The urge to void awakened her four or five times a night, leaving her exhausted every morning. With Detrol, taken twice a day, her bathroom visits have been cut in half and she can now control urges without having to worry about accidents. Although results with the drug are not always so dramatic, studies show the majority of patients benefit significantly. A second new drug, Ditropan XL, taken once a day reduced urge incontinence by 83 percent and eliminated it entirely in 43 percent of patients, according to a study of 256 patients reported in June to the American Urological Association. The manufacturer, Alza Corp., which developed the drug for Crescendo Pharmaceutical Corp., is awaiting marketing approval. Consumers seeking more information about overactive bladder can call 1-877-OVERACT (683-7228), a recorded hot line run by the Bladder Health Council of the American Foundation for Urologic Disease.

Treatments Offer Promise for Embarrassing Ailment By JANE E. BRODY Dec 8, 1998

 GLOSSARY OF MEDICAL TERMS

abdomen: the portion of the torso that includes the stomach, intestines, liver, gallbladder,

pancreas, and bladder

bladder: a muscular sac that stores urine

collagen: the protein found in connective and other tissues

diabetes mellitus: a disorder in which the body cannot process carbohydrates efficiently

electrodes: tiny devices attached to the body usually with an adhesive patch, and connecting to a

monitoring or stimulating machine

neurological: pertaining to the brain and spinal cord, the bodys main coordinating and controlling center

prolapsed: dropped or fallen from its normal position

prostate: a firm, walnut-sized gland near the bladder neck in men that produces the fluid in semen

urethra: the canal that carries urine from the bladder out of the body

urinary sphincter: the circular muscle around the urethra that helps control urination

urine: fluid made in the kidneys that travels to the bladder through the ureters and out of the body through the urethra

uterus: womb

\10 Yeast infections (candida)

Yeast Infections (Thrush) in the Child Care Setting Yeast infections are caused by various species of Candida, especially Candida albicans. These organisms are part of the germs normally found in various parts of the body and ordinarily do not cause any symptoms. Certain conditions, such as antibiotic use or excessive moisture, may upset the balance of microbes and allow an overgrowth of Candida. In most persons, these infections flare up and then heal. However, in newborns or persons with weak immune systems, this yeast can cause more serious or chronic infections.

Many infants get Candida infections from their mothers during birth. Many of those that escape this infection soon acquire Candida from close contacts with other family members and doting relatives and friends.

These early exposures may result in an oral infection (thrush) that appears as creamy white, curd-like patches on the tongue and inside of the mouth. In older persons, treatment with certain types of antibiotics or inhaled steroids (for asthma) may upset the balance of microbes in the mouth, allowing an overgrowth of Candida that will also result in thrush. Outbreaks of thrush in child care settings may be the result of increased use of antibi-otics rather than newly acquired Candida infections.

Candida may also exacerbate diaper rash, as this yeast grows readily on damaged skin. The infected skin is usually fiery red with lesions that may have a raised red border. Children who suck their thumbs or other fingers may occasionally develop Candida around their nails.

Oral thrush and Candida diaper rash are usually treated with the antibiotic nystatin. A corticosteroid cream can be applied to highly inflamed skin lesions on the hands or diaper areas. For children with diaper rash, child care providers should change the diaper frequently, gently clean the childs skin with water and a mild soap and pat dry. While cornstarch or baby powder may be recommended for mild diaper rash, it should not be used for children with inflamed skin. High absorbency disposable diapers may help keep the skin dry. Plastic pants that do not allow air to circulate over the diaper area should not be used although the diapering system should be able to hold urine or liquid feces.

Since most persons are already infected with Candida, children with thrush and candida diaper rash need not be excluded from child care as long they are able to participate comfortably. Child care providers should follow good hygiene including careful handwashing and disposal of nasal and oral secretions of children with thrush in order to avoid transmitting the infection to children who are not already infected.

 A vaginal yeast infection is also known as candidiasis or monilial vaginitis. It is estimated that three of four women will get a yeast infection at some time in their life, and that 1 in 2 will have more than one.

Candidiasis albicans normally lives in small numbers on the skin, in the mouth, in the intestines and in the vagina without causing any symptoms. When the fungus begins to grow too quickly it causes vaginal irritation and results in a yeast infection.

Any woman can get a yeast infection. Certain things may make a woman more likely to get a yeast infection. These include: use of antibiotics (antibiotics can kill the "good" bacteria in the vagina, and the yeast takes over) changes in hormones caused by pregnancy, menstrual period, or use of high dose birth control pills high amounts of sugar in the vagina from eating too many starches and sugars, or from diabetes a weakened immune system (the bodys defense against germs) caused by steroid medications, HIV infections, stress, or illness moisture and irritation of the vagina caused by panty-hose, tight pants, or underwear made of non-breathable cloth (such a nylon or lycra) poor hygiene such a wiping back to front after a bowel movement frequent douching, which can disturb the balance of the vagina obesity

SIGNS AND SYMPTOMS - The signs and symptoms of a yeast infection can include: itching and burning of the vagina and the outside of the vagina (the vulva) redness or rash on the vulva a white vaginal discharge that looks like cottage cheese. Pain during sex. Burning while pee.

DETECTION AND DIAGNOSIS - If a woman has never had a yeast infection before she should see a doctor because many other infections may cause symptoms like those of a yeast infection. Treating another type of infection with yeast infection medicine may make that infection much worse and there will be a delay in correct treatment. If a woman has repeated yeast infections and is familiar with the signs and symptoms, then talk to the doctor about over-the-counter meds.

The doctor will ask questions about the signs and symptoms, do a pelvic exam, and look at some of the vaginal discharge through a microscope to determine the seriousness of the yeast.

TREATMENT - If the woman has a yeast infection, the doctor will probably prescribe a nonprescription antifun-gal cream or suppository that is put directly into the vagina. There is also a new Rx one time pill (Fluconazol) that is effective in clearing up a yeast infection.

It is very important to finish all the med proscribed, even if the symptoms go away. If all the med is not taken, the yeast infection will probably come right back.

Symptoms usually are dramatically better in a few days. Contact the doctor if any of the following happens: abdominal pain. fever, discharge becomes foul smelling, symptoms no better after 3 days, symptoms come back in less than 2 mths.

No matter what cream or suppository is used to treat the yeast infection be sure to: read and follow directions, finish all med as ordered. Do not have sex during treat-ment. Wear a sanitary pad (med may be messy and seep out)

PREVENTION - There are some things women can do to avoid yeast infections: Wear loose, natural-fiber clothing and underwear with a cotton crotch Wear panty hose, tights, and leggings as little as possible Dont use deodorant tampons and feminine deodorant sprays. Dry off quickly after bathing and swimming - don't stay in a wet swimsuit for hours. Wipe from front to back after bowel movement. Use gentle soaps and unscented toilet paper and sanitary pads. Avoid douching. Practice good feminine hygiene. Wash the vulvar and anal areas with mild soap and water at least once daily, and wear clean underwear every day. Limit the amount of sweets and starches in the diet. Take steps to avoid getting "run down" such a getting enough sleep, eating right, and limiting stress.

candidiasis - cutaneous

fungal infection of the skin; skin infection - fungal; skin infection - yeast; skin yeast infection; yeast infection of the skin

An infection of the skin by the yeast-type fungus, Candida. The body normally hosts a variety of microorg-anisms including bacteria and fungi. Some of these are useful to the body. Others may multiply rapidly and form infections. Fungal infections are caused by microscopic plants (fungi) that can live on the skin. They can live on the dead tissues of the hair, nails, and outer skin layers. Fungal infections include mold-like fungi (derma-tophytes, which cause tinea infections) and yeast-like fungi (such as Candida).

Cutaneous candidiasis involves infection of the skin with Candida. It may involve almost any skin surface on the body. Cutaneous candidiasis is fairly common. Candida is the most common cause of diaper rash in infants where it takes advantage of the warm moist condition beneath the diaper. The two most commonly involved forms are Candida albicans and Candida tropicalis.

Candida infection is particularly likely during pregnancy or other conditions that involve hormone changes, and in diabetes and other endocrine disorders. It is also likely in people who are obese or who perspire freely because fungal infections, including Candida infections, thrive in warm moist 3environments. Antibiotics and oral contra-ceptives increase the risks. Oral thrush, a form of Candida infection found on the mucous membranes of the mouth, may be a sign of HIV infection or other immunode-ficiency disorders when it occurs in adults.

Candida infections are contagious and can be passed from direct contact or contact with items such as combs, clothing, shower or pool surfaces. Candida may also be transmitted sexually. It also can be transmitted from contact with pets that carry the fungus.

-- Treament  General hygiene is vital to the treatment of cutaneous candidiasis. Keep the skin clean and dry (see prevent-ion). Exposure to air as much as possible is helpful in drying the skin. If possible, discontinue antibiotics or other medications that may increase the risk of Candida infection. Topical or systemic antifungal medications may be used to treat the infection. Treatment may need to be prolonged.

Expectations (prognosis): Cutaneous candidiasis may be difficult to treat and require prolonged treatment. Recurrence is common. Complications: recurrence of Candida skin infection spread of Candida infection to other body areas formation of granulomas (granular tumors) systemic Candida infection, can be fatal (rare) disseminated candidiasis in immunocompromised individuals.

See your doctor if symptoms indicate a yeast infection.

 Prevention  Good general health and hygiene help prevent Candida infections. Keep the skin clean and dry. Loose-fitting clothing allows the skin to dry. Natural materials that "breathe" allow the skin to dry better than synthetic materials. Clothing, including socks and shoes, should be changed as often as necessary to keep the skin dry. Wash and dry the hands thoroughly after contact with any fungal infection, including contact to treat infection.

Wash and dry thoroughly any items that may contact an area with a fungal infection to avoid spread of the fungus spores. Antifungal or drying powders may help prevent fungal infections in people who are susceptible to them.

QUESTIONS TO ASK YOUR DOCTOR - Do I have a yeast infection or could the infection be another organism?

What treatment do you recommend?

How long will it take for relief of symptoms? What can I do about the itching and discomfort right now?

If I take antibiotics, what can I do to prevent an infection?

How can I prevent this from happening again?

The quandary of recurrent vaginal candidiasis - True recurrent candidal vaginitisrarer than many women may thinkcan be caused by an underlying deficiency in cell-mediated immunity or by an allergic response. Treatment should be based on the results of a comprehensive workup.

The lay press has popularized the ideanever proventhat candidal infections are the underlying cause of a multitude of symptoms in every body part. Consequently, most women who seek help for recurrent symptoms of vaginitis will claim to have a yeast infection.

Unfortunately, most of these self-attempted diagnoses are incorrectevidence of Candida is detected in subsequent examinations only 30% of the time. Not surprisingly, therefore, antifungal medications have no effect on most of these conditions. The terms chronic and recurrent vulvovaginitis are frequently confused. This can lead to inadequate treatment resulting from misinterpretation of the pathophysiology in a particular patient. Chronic infection almost always implies an active, persistent infectious process for prolonged periods. That does not seem to be the case in recurrent candidal vulvovaginitis, which usually occurs in repeated, acute, short-term episodes of variable intensity. Therefore, candidal vulvovaginitis can be recurrent but is not chronic.

The recurrences are chronic in a subgroup of women who have repetitive acute episodes over a long period. Differentiating between colonization and infection of the vaginal epithelium is also important. Many asymptomatic women are continually colonized with Candida albicans in the vagina, but this does not imply that a current, chronic, or even latent infection is present. Of private patients at our institutions, about 5% with an initial episode of candidal vaginitis have recurrent infection after apparently successful treatment with antifungal medications. To prevent frequent episodes, the physician must identify underlying factors that encourage Candida growth and then take measures to reduce these risks.

Pathophysiology More than 95% of candidal vaginal infections are caused by C albicans; the remainder are caused primarily by Candida glabrata and Candida tropicalis. Although all women have antibodies to Candida, these antibodies are nonprotective and do not prevent growth of the organism. Moreover, women with defective B-cell immunity do not have increased rates of vaginal candidiasis. Cell-mediated immunity appears to be the major, if not the only, immune mechanism limiting vaginal proliferation of C albicans. Polymorphonuclear leukocytes are not noticeably present in the vagina. Rather, mononuclear lymphoid cells, macrophages, and T lymphocytes appear to be major regulators of vaginal Candida growth.

Women who have genetic defects that affect T lymphocyte or macrophage functions have an increased rate of candidal mucous-membrane infections. In healthy women with normally functioning immune systems, infection of mucosal surfaces by Candida is readily treated and rarely recurs. Conversely, a defective in vitro cellular immune response to Candida is demonstrable in many women with recurrent candidal vaginitis. Physicians do not always appreciate that recurrent C albicans vaginal infections often are opportunistic and secondary to a transient deficiency in cell-mediated immunity.

An immune response by T helper (h) lymphocytes can occur along two pathways. A Th1 response results in release of cytokines that activate cell-mediated immunity (interferon-gamma, interleukin-1, interleukin-12), while a Th2 response results in release of different cytokines that stimulate antibody production (interleukins 1-4, 5, and 10). Women whose T cells manifest a Th2 response upon exposure to Candida because of genetic and/or environmental (allergic) factors are less likely to limit vaginal Candida proliferation and thus will be increasingly susceptible to repeated episodes of candidal vaginitis.

In about 20% of cases, a vaginal allergic response can be implicated as a predisposing factor for recurrent candidal vaginitis. Semen components, contraceptive spermicides, vaginal douches, other chemicals or medicines that may come into contact with the vagina, or C albicans itself, can serve as allergens in sensitized women. The vagina's immediate hypersensitivity response causes release of histamine, which stimulates macrophages to produce prostaglandin E2 (PGE2). This substance inhibits production of interleukin-2 by T lymphocytes, thereby transiently paralyzing the cell-mediated immune response. Under these conditions, Candida organisms, normally present at low levels in the vaginas of many women, are able to proliferate and trigger a clinical infection.

Allergy-related candidal vaginitis also can be induced in nonallergic women if the male partner has a genital tract allergic response. In these cases, IgE antibodies are transferred to the woman by coitus and bind to her basophils and mast cells. The allergen, also present in the ejaculate, then reacts with the bound IgE, initiating an allergic response.

Candidal vaginitis most often reappears during the late luteal phase of the menstrual cycle, when the elevated level of progesterone downregulates cellular immune response and lessens inhibition of Candida growth. Similarly, women with endocrinopathies also may be especially susceptible to recurrent candidal vaginitis.

Infectivity of C albicans is associated with the ability of the yeast forms to germinate. Recent evidence indicates that germination, too, may be regulated by cellular immune system components. Compounds such as PGE2, which increase the intracellular level of cyclic adenosine monophosphate (cAMP), promote Candida germination. Thus, medications that increase cAMP levels also may increase susceptibility to candidal vaginitis. Conversely, interferon-gamma, a product of activated T lymphocytes, inhibits it. C albicans can also be present in the male genital tract. Recurrent infection in a woman, therefore, sometimes may result from failure to eliminate the reservoir of infection in her male partner.

Diagnosis Recurrent candidal vaginitis may show the classical symptoms of pruritus, inflammation, and curdlike, cheesy discharge. Sometimes, intense pruritus may be the only symptom. Unfortunately, many patients have been treated by numerous physicians, nutritionists, and other health care providers and have tried various home remedies that often complicate and mask presenting symptoms. Therefore, the gross appearance of vaginal secretions is not diagnostic.

You can confirm diagnosis in some cases by finding branched, budding pseudohyphae on wet mounts of vaginal secretions in 10% potassium hydroxide. In many symptomatic patients in whom candidal infection is suspected but wet mounts are negative, a more sensitive and specific test is to inoculate Sabouraud dextrose agar slants with a vaginal swab. Identify the yeast as C albicans by inoculating a small colony into serum or glucose beef extract and examining for germ tube formation after 90 to 120 minutes.

Use of polymerase chain reaction (PCR) to detect Candida in vaginal specimens of symptom-atic women is also helpful. There is no relationship between yeast concentration and clinical symptoms. Some women with high colony counts may be asymptomatic. Others may have symptoms, but the organism is detectable only by the ultrasensitive PCR. This fact highlights the importance of host factors in candidal infections. If Candida is not detected, the patient should be screened for bacterial vaginosis as well as for Chlamydia trachomatis, human papillomavirus, and mycoplasma infections. Patients should be questioned about such classic risk factors as frequent antibiotic or steroid usage, pregnancy, diabetes or other endocrinopathies, poor perianal hygiene, or wearing tight clothing or nylon or silk undergarments. Typically, most patients will be negative for these risk factors.

Ascertain the relationship between sexual activity and vaginal symptoms. Are the symptoms temporally related to coitus with just the present partner or with all partners? Does the sexual partner have symptoms of genital, oral, or digital candidal infection? Was the partner taking any medication or drug to which the woman might be sensitized? What is the means of contraception? At our institution, women who have recurrent vaginitis are tested for evidence of a vaginal allergic response. We obtain a vaginal wash sample by instilling 5 to 10 mL of sterile saline into the vagina with a needle and syringe (directing the injection flow against the sidewalls), withdrawing the solution, and separating it into pellet and supernatant fractions by centrifugation. Enzyme-linked immunosorbent assay is used to test the supernatant for IgE antibodies to Candida and semen and the pellet for bound IgE. In coitus-related vaginitis, we obtain cultures for Candida from semen samples and test for total IgE and specific IgE antibodies to the vaginal wash pellet.

Although not performed routinely, a lymphocyte proliferation assay on a sample of peripheral blood mononuclear cells isolated from heparinized blood may be useful when immunosuppression is suspected, such as in women with concomitant oral thrush or condyloma. In such instances, a defective proliferative response to Candida and plant mitogens might indicate a more serious underlying disease.

Treatment The best treatment option for a patient with presumed chronic recurrent vaginal candidiasis depends on the appropriate comprehensive diagnosis. The two goals of treatment are to alleviate acute infectious symptoms and to avoid subsequent recurrences. Resistance to antifungal agents does not seem to be a problem for candidal vaginal infections. The majority of commercial products successfully treat acute fungal infections in most patients. At the present time no medication for clinical use is completely fungicidal. Treatment with antifungal agents reduces the number of vaginal organisms to a level undetectable by culture but does not achieve complete eradication of the organism in the vagina.

Many different approaches have been suggested for the treatment of women with chronic recurrent candidal vulvovaginitis (see Table 1). However, none is successful in every case. Between 25% and 40% of patients will have a clinical recurrence within 6 weeks if the second phase of treatmentthat is, maintenanceis not initiated. On the other hand, when maintenance treatment is given, most patients will be found to be free of symptoms for at least 6 months.

TABLE 1 Therapy for chronic recurrent candidal vaginitis

Drug* Regimen** INITIAL TREATMENT Clotrimazole, 1%, vaginal cream (Gyne-Lotrimin, Mycelex-G) OR Miconazole nitrate, 2%, vaginal cream (Femizol-M, Monistat 7) OR Fluconazole (Diflucan) 5 g intravaginally once daily for 10-14 d 5 g intravaginally once daily for 10-14 d 150 mg orally in a single dose

MAINTENANCE THERAPY Clotrimazole, 1%, vaginal cream OR Miconazole, 2%, vaginal cream OR Nystatin (Mycostatin), 100 000-unit vaginal tablets OR Itraconazole (Sporanox), 100-mg capsules OR Ketoconazole (Nizoral) OR Fluconazole, 100-mg tablets 5 g intravaginally once daily for 3-5 d before every menstrual period for 6 mo 5 g intravaginally once daily for 3-5 d before every menstrual period for 6 mo 1 tablet intravaginally every fourth night for 6 mo 1 capsule orally once daily for 6 mo 100 mg orally once daily for 6 mo 1 tablet orally every week for 6 mo *Other antifungal agents can also be used. **Treatment of acute infection should be longer than 2 to 3 d. If candidal vaginitis is associated with coitus with one particular partner, find out whether he is ingesting any medications or drugs that may enter his semen and elicit a vaginal response. Reports exist of vaginal allergic reactions to semen that contained products of ingested penicillin or thioridazine (Mellaril). Change or eliminate the offending medication, if possible. Similarly, evaluate the effect on vaginitis recurrence of changing the contraceptive method or spermicide brand. If the woman has vaginal fluid IgE antibodies to her partner's semen or the man has IgE antibodies in his ejaculate, using a condom will eliminate vaginal contact with the allergen. An untested alternative is the use of an oral antihistamine before intercourse.

Vaginal allergic responses to Candida appear to be relatively common in women with recurrent candidal vaginitis. In one study, we found that 18% of 64 patients tested had anticandidal IgE in their vaginal washes. In women who are hypersensitive to Candida or to an unidentified component of a vaginal wash sample, the best treatment at present is to prevent growth of Candida by aggressive use of antifungal agents plus use of oral antihistamines to obtain symptomatic relief of vaginal symptoms and reduce the incidence of histamine-mediated immunosuppression. Hyposensitizing the patient to Candida, semen, or any other allergen associated with a vaginal allergic response may ultimately provide the best therapy. However, improved methodology and standardization, along with controlled clinical trials, are needed to evaluate the effectiveness of these experimental immunizations.

- Internal Medicine Archive Assessing and managing vaginitis This common gynecologic problem can be appropriately managed in nearly all primary care settings. Here's an overview of the various causes of vaginitis, physical examination of the patient, and treatment options. By Roger P. Smith, MD

Vaginitis is one of the most common gynecologic problems you'll encounter in your practice as an internist. Women with this condition, which is characterized by vaginal discharge and irritation, account for more than 10% of all outpatient visits to gynecologists. They may present with acute, subacute, or indolent symptoms ranging from minimal to incapacitating. Though generally nonspecific, the patient's history and signs and symptoms may point to chemical, allergic, or other causes besides infection. Irritation of the well-innervated tissues of the vulva often causes intense pruritus. Edema, induration, and localized lesions, such as those seen in herpes infections, may be present. In almost all primary care settings, it's important that the internist diagnose and treat vaginitis promptly. Rarely will it be necessary for you to refer the patient to a specialist for evaluation. In this article, I'll discuss the three infectious causes of vaginitis, the physical examination of the patient, and appropriate treatment of this condition in its various forms.

Rich bacterial flora Vaginal secretions are always present to some extent, the amount and character being dependent on chemical, mechanical, and pathologic conditions. The vaginal canal has a rich bacterial flora and unique fluid dynamic. Healthy women of reproductive age produce about 1.6 to 4.8 grams of vaginal secretions a day, consisting of shed vaginal epithelium (responsible for the characteristic creamy white, slightly curdy character), cervical mucus and vaginal transudate (creating the moisture), and trace amounts of material from accessory sex glands. The natural lubrication provided by these secretions helps prevent drying and irritation of the vaginal canal. Normal vaginal secretions have no odor, although some slight aroma may be detected on careful examination. Bacteria are usually found in concentrations of 108 to 109 colonies/mL of vaginal fluid. Because the vagina is a potential space, a ratio of 5:1 anaerobic to aerobic bacteria is typical. This profusion of diverse organisms means that cultures of the vaginal canal are rarely of any help clinically and generally should not be performed. The normal pH of the vagina is between 3.5 and 4.5. It's higher (between 6 and 8) in premenarchial girls and postmenopausal women, who have lower levels of glycogen.

Serious health risk Vaginal infections can be more than inconvenient and uncomfortable; they can represent a serious health risk. Patients with bacterial vaginosis are roughly nine times more likely to develop upper genital tract infections than uninfected women. Premature rupture of the membranes, premature delivery, chorioamnionitis, and postpartum endometritis are all more common in the presence of bacterial vaginosis. The incidence of bladder infections and postoperative cuff cellulitis also increases. Multiple pathogens can cause vaginal infections, but the most common are Candida, Trichomonas vaginalis, and shifts in microbiologic flora associated with bacterial vaginosis. In terms of susceptibility, a woman's age may be a significant factor in fighting off these pathogens and preventing infection. The thicker, more robust vaginal tissues found during the reproductive years are more resistant to infection than are those of premenarchial girls and postmenopausal women.

Common pathogens in vaginitis Candida albicans on vaginal epithelium Trichomonas and epithelial cells

Foreign bodies may cause a major infection and discharge. While we tend to associate this problem with young and elderly women, it may occur at any age. Foreign bodies may range from bits of toilet paper, condoms, diaphragms, or retained tampons, to iatrogenic items such as pessaries, to more sinister objects suggesting abuse, neglect, or psychopathology. As noted above, the patient's history and symptoms are typically nonspecific, but a careful history-taking may uncover potential causes that warrant investigation. The history should cover hygiene and sexual practices, and the physical examination must be thorough. In 80% to 90% of cases of increased vaginal discharge, a microbiologic process can be identified as the cause. Hormonal and chemical factors account for the remaining cases.

Three infectious causes Most vaginal infections result from three infectious causes: synergistic bacteria (bacterial vaginosis, nonspecific vaginitis), fungi (candidiasis), or protozoa such as Trichomonas (trichomoniasis). Bacterial infections account for approximately 50% of infections; fungal and trichomonal infections account for roughly 25% each.

The etiology of the patient's symptoms may be ascertained through the history, physical examination, and simple microscopic investigation. Empiric diagnosis or treatment has been proven to be highly inaccurate and ineffective. For this reason, any patient who complains of vaginal discharge or irritation must be evaluated directly before therapy is suggested. An inaccurate diagnosis, or overtreatment of a physiologic condition, is doomed to fail and may even make the patient worse.

The examination of the woman with increased vaginal discharge, leukorrhea, vaginal or vulvar irritation, or increased odor should include careful observation of the tissues and discharge. Note the location, color, consistency, odor, and pH of the discharge. The pH of the vaginal secretions is an often overlooked tool that may be helpful in establishing the correct diagnosis. Vaginal pH can be easily measured with commercially available pH tapes. Keep in mind, however, that vaginal pH may be unreliable in the presence of blood or after recent douching or intercourse.

Bacterial vaginosis often asymptomatic Bacterial vaginosis may affect up to 20% of all women. The high prevalence is supported by a number of studies and the observation that 50% of patients with bacterial vaginosis are asymptomatic. Thus, the condition is not clinically apparent. Symptomatic cases are characterized by a creamy, gray-white, adherent vaginal discharge, with an increased odor that is often "musty" or "fishy" in nature and is more noticeable after intercourse. Bacterial vaginosis is a diagnosis that has undergone a great deal of change and debate in the last few years. Once thought to be caused by the infection of Gardnerella vaginalis (formerly called Haemophilus or Corynebacterium vaginale), most clinicians now feel that bacterial vaginosis is actually a symbiotic infection of anaerobic bacteria (Bacteroides sp, Peptococcus sp, or Mobiluncus sp) and Gardnerella, both of which contribute to the clinical findings.

The discharge is gray-white and may be frothy in 10% of cases. The diagnosis can be confirmed by a saline wet smear showing more than 20% "clue cells." (Clue cells are normal vaginal epithelial cells with small bacilli adhering to their surfaces, giving a ground-glass appearance to the cytoplasm. True clue cells may be distinguished by their fuzzy borders as well as their granular appearance.) A Gram's stain, or stains used for urinary sediments, may help identify these cells, but this is seldom necessary.

Treating bacterial vaginosis Bacterial vaginosis may be treated with oral or topical therapy (Table 3). Oral metronidazole (Flagyl, Protostat) yields 90% to 100% cure rates. It carries the risk of systemic side effects, including a metallic taste in the mouth and stomach upset. And because of a disulfiram-like reaction, patients should be warned to avoid alcohol intake during therapy. Oral ampicillin, tetracycline, or clindamycin may also be prescribed, but their cure rates are not as good as metronidazole's. Topical therapy for bacterial vaginosis can give excellent results with fewer risks of systemic side effects. Topical triple sulfa (cream or suppositories) has fallen out of favor. It's been replaced by topical clindamycin (2% cream) and metronidazole (0.75% gel). Both agents have slight systemic absorption (1% to 5%), so systemic effects are possible but unlikely. Cure rates are comparable to oral therapy. Currently, treatment of the patient's sexual partner is not advised.

Ubiquitous fungi Candidal vulvovaginitis accounts for 25% to 40% of all vaginal infections. It's been estimated that 75% of women will experience at least one episode of candidal vulvovaginitis during their lifetimes. This condition is caused by ubiquitous fungi found in the air or as common inhabitants of the vagina, rectum, and mouth. Most infections (80% to 95%) are caused by Candida albicans; infections caused by Candida glabrata, Candida tropicalis,and other organisms account for the remaining 5% to 20% of cases.

When the normal ecosystem of the vagina is disturbed-by stress, antibiotics, pregnancy, diabetes, depressed immunity, or contraceptive sponge use, for example-rapid fungal overgrowth may occur, with organism levels reaching 103 to 104/mL. Depressed cellular immunity, such as that caused by corticosteroids or AIDS, significantly increases the likelihood of infection. Candidal infections are not considered sexually transmitted and are not associated with a greater risk of other infections. Candidal vulvovaginitis occurs almost exclusively between menarche and menopause. Its cardinal sign is intense itching; external dysuria, dyspareunia, and vulvar burning are also common. Hypersensitivity to the organism may contribute to the severity of symptoms found in even mild infections. Tissue erythema, edema, and excoriations are common.

The discharge associated with these infections is usually very adherent, thick, and curdy, with a white to yellow color, and generally odorless. The pH of the vagina is usually normal. Microscopic examination of vaginal secretions will often show hyphae; using 10% KOH, which lyses white and red blood cells, will make the hyphae more apparent. Fungal cultures with Nickerson's or Sabouraud's media should be positive in 24 to 72 hours, but this test is generally reserved for difficult or recurrent cases.

Synthetic imidazoles: Preferred treatment The most commonly prescribed drugs for vaginal fungal infections are the synthetic imidazoles (Table 3). These agents all provide good symptomatic relief and microbiologic cures; less than 5% of fungal infections will be resistant to imidazole therapy. Triazole-based medications, such as terconazole (Terazol) or fluconazole (Diflucan), may also be used. Side effects from either type of therapy are mild and relatively infrequent. Other reasonable therapies for candidal vulvovaginitis are povidone-iodine (as a douche or gel), gentian violet (1%), and boric acid capsules. The choice of oral versus vaginal therapy should be a matter of patient and physician preference. Roughly 30% of patients will experience a recurrence of symptoms within a month.

Topical suppressive therapy, the use of oral nystatin, perianal creams, and medications for sexual partners have not been successful in reducing the recurrence rate. For the few patients who have chronic recurrences, monthly oral suppressive therapy does appear to lessen the frequency and severity of these episodes. Prophylactic use of antifungals during broad-spectrum antibiotic therapy or around the time of menstruation is controversial, but it may be appropriate based on the patient's history and needs. Frequent recurrences should prompt further evaluation of the patient for diabetes or immunosuppression.

Sexual transmission of trichomoniasis Though decreasing in frequency due to effective treatment and aggressive diagnosis, vaginal infections from T vaginalis still account for up to 3 million cases of vaginitis each year in the US. An anaerobic flagellate protozoan, T vaginalis lives only in the vagina, Skene's ducts, and urethra (male or female), and may be freely transmitted through sexual intercourse. Studies have found that 30% to 80% of asymptomatic partners of women with trichomoniasis will have a positive culture. Up to 15% of women may harbor T vaginalis in an asymptomatic, carrier state, so the exact time of exposure may be difficult to determine. But the incubation period for these infections is thought to be between four and 28 days.

Because transmission of the disease is predominately sexual, you need to consider the possibility of other STDs and conduct appropriate screening tests. Symptoms of trichomoniasis range from mild to severe and may include vulvar itching or burning, copious discharge with a rancid odor, dysuria, and dyspareunia. Although not present in all women, the discharge associated with these infections is generally thin and yellow-green to gray in color. In 25% of patients, it will take on a frothy character. The vaginal pH is approximately 6 to 6.5 or above. On examination, you may find nonspecific edema or erythema of the vulva. Characteristic petechiae, or "strawberry patches," are found on the upper vaginal wall or cervix in 10% to 15% of patients and are highly suggestive but not diagnostic.

Confirmation of the diagnosis requires microscopic examination of vaginal secretions suspended in normal saline. The organism is a fusiform protozoa with three to five flagella extending from its narrow end. The active movement of these flagella make Trichomonas easy to identify. A culture may be performed but is seldom necessary. Detection by Papanicolaou smear carries an error rate of 50%. Monoclonal antibody kits are available, but they're expensive and have not shown any superiority over traditional diagnostic methods.

Metronidazole is standard treatment The standard treatment for trichomoniasis is metronidazole, which may be given as a single-day oral treatment or extended over seven days (Table 3). Both forms of therapy yield comparable cure rates, but the cost and side effects are lower with single-day therapy. Metronidazole is relatively contraindicated in the first trimester of pregnancy, when alternate therapies must be used. These include topical clotrimazole, povidone- iodine, or hypertonic (20%) saline douches. Because of its sexual transmission and association with other STDs, most clinicians recommend treating asymptomatic sexual partners at the same time. Resistance to metronidazole is uncommon. When therapy proves unsuccessful, it's usually due to reinfection or the patient's failure to comply with treatment.

Evaluating chronic vaginitis A bane of physicians and patients alike is chronic or recurrent vaginitis. Women experiencing this condition complain, often bitterly, of persistent vaginal discharge, odor, or both, with no readily identifiable cause or satisfactory response to treatment. They claim to have "tried everything," visiting several physicians without success. With these patients, you need to be especially thorough in your history-taking. Explore past medical conditions, as well as hygiene and sexual practices. A methodical physical examination and microscopic evaluation are also required. Besides investigating the usual causes of vaginitis, remember to consider other possible explanations for the patient's complaints. Victims of sexual assault, whether recent or past, for example, may present in this manner. If the woman has recurrent infections, you'll need to provide a frank explanation of the risk of reinfection. The number of sexual partners (of the patient and her significant other) should be explored in a nonjudgmental manner. Also evaluate alternate sources of excessive vaginal moisture such as chronic cervical infections. In managing patients with chronic vaginitis, the cornerstone of treatment is an accurate diagnosis. Treatment without a definite diagnosis risks making the problem worse. Once a cause has been identified, specific therapy should be initiated with emphasis on the need for compliance. The patient should return shortly after completion of therapy for reevaluation, even if no symptoms are present. This allows for objective tests of cure and underscores the importance of compliance. Prolonged therapies, prophylaxis, or vaginal acidification may all be required. If the patient's complaints seem to exceed her physical and microscopic findings, the possibility of inappropriate expectations, inaccurate information, or psychologic dysfunction must be entertained. Patients may overreact to the presence, amount, or character of vaginal discharge out of fear, guilt, or a misconception about its significance. Somatization or fixation may be manifestations of depression or bipolar disorders. In summary, any internist who cares for women will encounter the complaint of vaginitis and must be prepared to provide necessary care. Diagnosing the cause and initiating prompt treatment are appropriate in almost all primary care settings.

TABLE 3: Treatment regimens for vaginitis Bacterial vaginosis Oral metronidazole 500 mg 2 * /day for 7 days ampicillin 500 mg q6hr for 7 days tetracycline 250-500 mg 2 * /day for 7 days clindamycin 300-450 mg q6hr for 7 days Topical metronidazole (5 gm cream, 37.5 gm metronidazole) applied 2 * /day for 5 days clindamycin (5 gm cream, 100 mg clindamycin) applied nightly for 7 days Candidal vulvovaginitis Oral synthetic imidazoles synthetic triazoles (terconazole, fluconazole) Topical/vaginal povidone-iodine (douche or gel) gentian violet (1%) boric acid, 600-mg capsules, inserted high in vagina 2 * /day Trichomoniasis Oral metronidazole, single-day treatment of 1 gm in morning and 1 gm in evening, or 250 mg q8hr for 7 days Topical/vaginal clotrimazole povidone-iodine hypertonic (20%) saline douches

Roger P. Smith, MD Dr. Smith is professor and chief, section of general obstetrics and gynecology, department of obstetrics and gynecology, The Medical College of Georgia, Augusta. Copyright  1997 and published by Medical Economics Company at Montvale, NJ 07645-1742. All rights reserved.