polymyositis

What is polymyositis?

Polymyositis is a disease of muscle featuring inflammation of the muscle fibers. The cause of the disease is not known. It begins when white blood cells, the immune cells of inflammation, spontaneously invade muscles. The muscles affected are typically those closest to the trunk or torso. This results in weakness that can be severe. Polymyositis is a chronic illness with periods of increased symptoms, called flares or relapses, and minimal or no symptoms, known as remissions.

Polymyositis is slightly more common in females. It affects all age groups, although its onset is most common in middle childhood and in the 20s. Polymyositis occurs throughout the world. Polymyositis can be associated with skin rash and is then referred to as "dermatomyositis." It also can affect other areas of the body and is, therefore, referred to as a systemic illness. Occasionally, it is associated with cancer or with other diseases of connective tissue (see systemic lupus erythematosus, scleroderma and rheumatoid arthritis).

What causes polymyositis?

To date, no cause of polymyositis has been isolated by scientific researchers. There are indicators of heredity (genetic) susceptibility that can be found in some patients. There is indirect evidence of infection by a virus that has yet to be identified in a form of polymyositis that is particularly resistant to treatment, called inclusion body myositis. This form of polymyositis is diagnosed by the pathologist, a physician specialist who interprets the microscope findings of muscle tissue. The muscle tissue in this form of polymyositis displays clear areas within the muscle cells (called vacuoles) when viewed under the magnification of a microscope.

Researchers from Sweden at the national meeting of the American College of Rheumatology in 2007 reported their findings that T-cells of the immune system in some polymyositis or dermatomyositis patients reacted against cytomegalovirus (CMV) and that detectable antibodies against CMV were present. Their conclusion was that there may be subsets of patients who develop their disease, in part, because of infection with this particular virus.

Aside from diseases with which polymyositis can be associated (as mentioned above), many other diseases and conditions can mimic polymyositis. These include nerve-muscle diseases (such as muscular dystrophies), drug toxins (such as alcohol, cocaine, steroids, colchicine, hydroxychloroquine, and cholesterol-lowering drugs, called statins), metabolic disorders (where muscle cells are unable to process chemicals normally), hormone disorders (such as abnormal thyroid), calcium and magnesium conditions, and infectious diseases (such as influenza virus, AIDS, streptococcus and Lyme bacteria, pork tapeworm and schistosomiasis).

Complications

Possible complications of polymyositis include:

• Difficulty swallowing. If the muscles in your esophagus are affected, you may have problems swallowing (dysphagia), which in turn may cause weight loss and malnutrition.
• Aspiration and pneumonia. Difficulty swallowing may also lead to entrance of food or liquids, including saliva, into your lungs (aspiration), which can lead to pneumonia.
• Breathing problems. If your chest muscles are affected by the disease, you may experience breathing problems, such as shortness of breath or in severe cases, respiratory failure.
• Calcium deposits. Late in the disease, particularly if you've had the disease for a long time, deposits of calcium can occur in your muscles, skin and connective tissues (calcinosis).

Associated conditions
Although these are not complications, polymyositis is often associated with other conditions that may cause further complications of their own, or in combination with polymyositis symptoms. Associated conditions include:

• Raynaud's phenomenon. This is a condition in which your fingers, toes, cheeks, nose and ears turn pale when exposed to cold temperatures.
• Other connective tissue diseases. Other conditions, such as lupus, rheumatoid arthritis, scleroderma and Sjogren's syndrome, can occur in combination with polymyositis.
• Cardiovascular disease. Polymyositis may cause the muscle of your heart to become inflamed (myocarditis). In a small number of people who have polymyositis, congestive heart failure and heart arrhythmias may develop.
• Lung disease. A condition called interstitial lung disease may occur with polymyositis. Interstitial lung disease refers to a group of disorders that cause scarring (fibrosis) of lung tissue, making lungs stiff and inelastic. Signs and symptoms include a dry cough and shortness of breath.

Tests and diagnosis

Diagnosis of polymyositis isn't always easy and can be a lengthy process. Even though the attempt to diagnose your condition may be frustrating, remember that an accurate diagnosis is necessary to receive appropriate treatment.

In addition to a thorough physical exam, your doctor will likely use other tests to confirm a diagnosis of polymyositis.

Imaging tests

• Magnetic resonance imaging (MRI). A scanner creates cross-sectional images of your muscles from data generated by a powerful magnetic field and radio waves.

  As MRI has become more sensitive, doctors have been using it more to diagnose inflammatory myopathies. MRI can detect active inflammation in your muscles, fibrosis and calcification. Its high sensitivity can detect subtle muscle inflammation and swelling early in the disease. A benefit of MRI is that it can look at large amounts of muscle to look for patterns or patches of muscle weakness, instead of taking a small sample from a single muscle, for example.

Muscle tests

• Electromyography. A doctor with specialized training inserts a thin needle electrode through the skin into the muscle to be tested. Electrical activity is measured as you relax or tighten the muscle, and changes in the pattern of electrical activity can confirm a muscle disease. The doctor can determine the distribution of the disease by testing different muscles.
• Muscle biopsy. A small piece of muscle tissue is removed surgically for laboratory analysis. A muscle biopsy may reveal abnormalities in your muscles, such as inflammation, damage or infection. The tissue sample can also be examined for the presence of abnormal proteins and checked for enzyme deficiencies. In polymyositis, a muscle biopsy typically shows inflammation, dead muscle cells (necrosis), and degeneration and regeneration of muscle fibers.

Blood tests

• Blood analysis. A blood test will let your doctor know if you have elevated levels of muscle enzymes, such as creatine kinase (CK) and aldolase. Increased CK and aldolase levels can indicate muscle damage. A blood test can also detect specific autoantibodies associated with different symptoms of polymyositis, which can help in determining the best medication and treatment.

Treatments and drugs

Although there's no cure for polymyositis, treatment can improve your muscle strength and function. The earlier treatment is started in the course of polymyositis, the more effective it is, leading to fewer complications.

Drugs

• Corticosteroids. These medications suppress your immune system, limiting the production of antibodies and reducing muscle inflammation, as well as improving muscle strength and function. Corticosteroids, especially prednisone, are usually the first choice in treating inflammatory myopathies such as polymyositis.

  Your doctor may start with a very high dose, and then decrease it as your signs and symptoms improve. Improvement generally takes about two to four weeks, but therapy is often needed for years.

  Prolonged use of corticosteroids can have serious and wide-ranging side effects, so your doctor may recommend supplements to combat them, such as calcium and vitamin D, and may prescribe bisphosphonates, such as alendronate (Fosamax), risedronate (Actonel) or zoledronic acid (Reclast). Bisphosphonates in pill form may not be recommended if you have difficulty swallowing.

• Corticosteroid-sparing agents. Your doctor may recommend other medications, either to decrease side effects or if your condition doesn't respond to corticosteroids. These medications include azathioprine (Imuran) or methotrexate (Rheumatrex). Your doctor may prescribe these alone or in combination with corticosteroids.

  When in combination, these additional immunosuppressants can be used to lessen the dose and potential side effects of the corticosteroid. Immunosuppressants, such as cyclophosphamide (Cytoxan) and cyclosporine (Neoral, Sandimmune), may improve signs and symptoms of polymyositis and interstitial lung disease.

Antibody therapy

• Intravenous immunoglobulin (IVIg). Immunoglobulin contains healthy antibodies from blood donors. High doses can block the damaging antibodies that attack muscle in polymyositis.

Immunosuppressive therapies
In addition to corticosteroids and immunosuppressive drugs, other treatments to suppress your immune system include:

• Tacrolimus (Prograf). This transplant-rejection drug may work to inhibit the immune system. Tacrolimus is often used topically to treat dermatomyositis and other skin problems. When taken orally, it may be helpful in treating people who have polymyositis complicated by interstitial lung disease.

Investigational treatment

• Biological therapies. Rituximab (Rituxan) has been studied in small numbers of people with polymyositis and dermatomyositis and shown to improve muscle strength, lung involvement and skin rash. Tumor necrosis factor (TNF) inhibitors such as etanercept (Enbrel) and infliximab (Remicade) have not been shown to be effective in trials with small numbers of people with polymyositis or dermatomyositis. Rituximab is not approved by the Food and Drug Administration for the treatment of polymyositis, so your insurance company will likely require preapproval if you wish to be reimbursed.

Other treatment

• Physical therapy. A physical therapist can show you exercises to maintain and improve your strength and flexibility and advise an appropriate level of activity.
• Dietetic assessment. Later in polymyositis, chewing and swallowing can become more difficult. A registered dietitian can teach you how to prepare easy-to-eat foods.
• Speech therapy. If your swallowing muscles are weakened by polymyositis, speech therapy can help you learn how to compensate for those changes.

Psoriatic arthritis

Definition

Psoriatic arthritis is an immune-mediated (autoimmune), connective tissue disease that is associated with a skin disorder marked by bumps and scaling (psoriasis) and is characterized by inflammation of the ligaments, tendons, fascia, and joint capsules (enthesitis) of the upper extremities, especially the hands. Small joints of the feet and large joints of the legs such as hips, knees, and ankles may be also involved. Most commonly, psoriatic arthritis affects fewer than five joints. Its arthroscopic symptoms and clinical findings are similar to those of rheumatoid arthritis, but it differs in its high frequency of distal joint involvement (joints farthest from the center of the body, such as small joints of hands and feet) and the serum of affected individuals is negative for rheumatoid factor.

Psoriatic arthritis occurs in five general patterns: arthritis affecting the small distal joints of toes and fingers (distal interphalangeal arthropathy), asymmetrical oligoarticular arthritis of the extremities, symmetrical polyarthritis that resembles rheumatoid arthritis, deforming and destructive arthritis (arthritis mutilans) with resorption of bone (osteolysis) and dissolution of the joint, and arthritis of the spine and sacroiliac joints (psoriatic spondylitis). These patterns may change in an individual over time.

The etiology of psoriatic arthritis is unknown, but genetic, immunologic and less conclusively, environmental factors such as infection and trauma are considered important components. The disease is associated with increased frequency of certain human leukocyte antigens (including HLA-B27, HLA-DR4m -DR7, and –Cw6) in the tissue of those affected with psoriasis and/or psoriatic arthritis. Genome scans have shown linkages to specific gene loci. Serum levels of immunoglobulins (IgA and IgG) are higher in psoriatic arthritis patients. Psoriasis is present years before the onset of arthritis in about 70% of individuals with psoriatic arthritis; 10% to 15% develop psoriasis and arthritis simultaneously, and 15% to 20% have arthritis before skin involvement (Ruderman). Risk: Individuals with psoriasis are at greatest risk for developing psoriatic arthritis; approximately 5% to 8% of individuals with psoriasis develop psoriatic arthritis (Hammadi). In contrast to rheumatoid arthritis, which affects women more than men, psoriatic arthritis shows no gender preference. Psoriatic arthritis usually occurs in individuals between ages 35 and 55 years, but can develop at any age. Risk is greater among whites than other races. A family history of psoriatic arthritis is a risk factor for developing the disease. Incidence and Prevalence: Incidence of psoriatic arthritis in the general population is estimated to be 1%; about 1 million adults in the US are affected (Hammadi) compared to 2 million with rheumatoid arthritis (Hammadi). Although incidence varies among countries, the incidence of psoriatic arthritis internationally ranges from 1% to 40% depending on the clinical criteria applied and whether all races are included (Van Voorhees). Prevalence is higher among whites than among African Americans and Native Americans; the disease occurs in 2.5% of white North Americans and 0.05% to 0.24% in the international white population (Hammadi).

Source: Medical Disability Advisor

Diagnosis

History: The individual may describe a family history of psoriasis or psoriatic arthritis. The individual may complain of pain, stiffness, and swelling of the joints, especially the small joints of the hands and feet. Depending on the area affected by psoriatic arthritis, other complaints may include back pain, chest pain, pain on walking or climbing stairs, pain around the eyes, and shortness of breath. Humidity and temperature changes may affect arthritis symptoms. Fever may be present in patients with the arthritis mutilans subtype of psoriatic arthritis. Individual may report that psoriasis has been present for some time before arthritis symptoms or that psoriasis developed at the same time as arthritis symptoms. The physician will obtain a history of recent and prior illness, particularly bacterial or viral infections. Physical exam: Psoriasis is usually present but may be limited to patches (lesions) between the buttocks, behind the ears, or other inconspicuous areas such as the umbilicus or scalp; psoriasis can be severe in some individuals. Swelling may be seen as well as deformity of the joints, especially finger joints in severe, chronic cases. Overgrowth of bone (hyperostosis) may be seen. "Sausage digits" (dactylitis) of the hands and feet are common in individuals with psoriatic arthritis. Affected joints often have a purplish discoloration. An accumulation of fluid may be seen in a joint (effusion). Nails of the affected digits may be pitted or crumbling (onycholysis). Inflammation of the outer membrane of the eyes (conjunctivitis) or the uveal tract (uveitis) may occur in up to 30% of individuals with psoriatic arthritis (Van Voorhees). Tests: There is no specific diagnostic test for psoriatic arthritis; observing the pattern of joint involvement is essential to correct diagnosis. Blood tests that may be helpful in making the diagnosis include erythrocyte sedimentation rate and C-reactive protein to evaluate inflammation, hemoglobin, rheumatoid factor (to rule out rheumatoid arthritis), uric acid (to rule out gout), human leukocyte antigen (HLA) typing, and antinuclear antibodies. A sample of joint fluid may be analyzed to determine the number and type of white blood cells. A cytokine profile may be done to assess T cell and monocyte activation, which may help differentiate between psoriatic arthritis and rheumatoid arthritis. X-rays usually are done to help differentiate psoriatic arthritis from other types of arthritis based on degree of joint erosion. Depending on areas affected and symptoms reported by the individual, either CT or MRI imaging can be done to examine soft tissue and joint characteristics in more detail. CT scans of the sacroiliac joint are considered to be sensitive for viewing spondylitis or sacroiliitis. MRI is especially sensitive for assessing pathology of the hands and feet.

Treatment

Treatment of the polyarthritis component focuses on controlling inflammation. It is subdivided into nonpharmacological, pharmacological, and surgical therapies. Nonpharmacological therapies include rest, wearing of splints over the affected joints, joint protection, and physical therapy. Pharmacological measures include nonsteroidal/anti-inflammatory drugs (NSAIDs), occasional corticosteroid injections into the joints, disease modifying antirheumatic drugs (DMARDs), and newer, injectable biologic agents that target tissue necrosis factor (TNF) and other cytokines. Surgery (hip or knee replacement) may be indicated in severe cases.

The psoriasis component is treated with topical therapy, systemic medications, and photochemotherapy (psoralen plus UV light). Treatment is individualized and depends on the size and location of psoriasis plaques. Immunosuppressive drugs (e.g., methotrexate) and retinoic-acid derivatives may be given in cases of severe skin involvement. These drugs have demonstrated effectiveness for both skin and joint symptoms. Cyclosporine, an antibiotic, has also demonstrated good results for psoriasis and psoriatic arthritis although it has toxic effects in some individuals.

Exercise is an important component of a treatment plan for psoriatic arthritis, resulting in reduced pain, swelling, and stiffness. Sufficient rest is also required.

Source: Medical Disability Advisor

Prognosis

Many individuals with psoriatic arthritis have mild disease with episodic flares and remissions. Because psoriatic arthritis is a chronic disease, joint deformities and movement limitations may increase over time. However, most individuals can maintain reasonable function of the affected joints. Medication can lead to periods of symptom remission. Individuals with many affected joints (polyarthritis), a family history of arthritis, early onset (younger than 20 years of age), or severe skin psoriasis have a poorer prognosis. Inflammatory arthritis of the spine (spondylitis) may develop in some individuals. Some will progress to a severe stage characterized by joint disintegration (lysis) or immobility (ankylosis).

gout

What is gout?

Gout is a kind of arthritis. It can cause an attack of sudden burning pain, stiffness, and swelling in a joint, usually a big toe. These attacks can happen over and over unless gout is treated. Over time, they can harm your joints, tendons, and other tissues. Gout is most common in men.

What causes gout?

Gout is caused by too much uric acid in the blood. Most of the time, having too much uric acid is not harmful. Many people with high levels in their blood never get gout. But when uric acid levels in the blood are too high, the uric acid may form hard crystals in your joints.

Your chances of getting gout are higher if you are overweight, drink too much alcohol, or eat too much meat and fish that are high in chemicals called purines. Some medicines, such as water pills (diuretics), can also bring on gout.

What are the symptoms?

The most common sign of gout is a nighttime attack of swelling, tenderness, redness, and sharp pain in your big toe . You can also get gout attacks in your foot, ankle, or knees. The attacks can last a few days or many weeks before the pain goes away. Another attack may not happen for months or years.

See your doctor even if your pain from gout is gone. The buildup of uric acid that led to your gout attack can still harm your joints.

How is gout diagnosed?

Your doctor will ask questions about your symptoms and do a physical exam. Your doctor may also take a sample of fluid from your joint to look for uric acid crystals. This is the best way to test for gout. Your doctor may also do a blood test to

measure the amount of uric acid in your blood.

How is it treated?

To stop a gout attack, your doctor can give you a shot of corticosteroids, or prescribe a large daily dose of one or more medicines. The doses will get smaller as your symptoms go away. Relief from a gout attack often begins within 24 hours if you start treatment right away.

To ease the pain during a gout attack, rest the joint that hurts. Taking ibuprofen or another anti-inflammatory medicine can also help you feel better. But don't take aspirin. It can make gout worse by raising the uric acid level in the blood.

To prevent future attacks, your doctor can prescribe a medicine to reduce uric acid buildup in your blood. If your doctor prescribes medicine to lower your uric acid levels, be sure to take it as directed. Most people continue to take this medicine for the rest of their lives.

Paying attention to what you eat may help you manage your gout. Eat moderate amounts of a healthy mix of foods to control your weight and get the nutrients you need. Avoid regular daily intake of meat, seafood, and alcohol (especially beer). Drink plenty of water and other fluids.

Reiter’s syndrome

Reiter’s syndrome: Introduction

Reiter's syndrome is a rare type of arthritis that causes inflammation of the urinary tract, eyes, skin, mucus membranes, and joints. Reiter's syndrome, also called reactive arthritis, is believed to occur as a reaction to certain infections of the reproductive system and the digestive system.

Infections that can lead to the complication of Reiter's syndrome include a common sexually transmitted disease called chlamydia. This is the most common cause of Reiter's syndrome. A less common cause of Reiter's syndrome is food poisoning due to Salmonella, Shigella, Yersinia or Campylobacter infection. Why some people develop Reiter's syndrome in reaction to these infections and other people don't is not known, but having a certain genetic factor called HLA-B27 increases a person's chance of developing Reiter's syndrome.

Hallmark symptoms of Reiter's syndrome affect the urinary tract, eyes, skin, mucus membranes, and joints. Complications include the development of chronic arthritis. For details about additional important complications and symptoms, refer to symptoms of Reiter's syndrome.

Making a diagnosis of Reiter's syndrome begins with taking a thorough medical history, including symptoms and history of Chlamydia infection or food poisoning, and completing a physical examination. A referral is generally made to a rheumatologist for definitive diagnosis and treatment. There is no specific test that can diagnose Reiter's syndrome. Diagnosis is made by evaluating the symptoms and interpreting them in conjunction with tests that rule out other diseases and conditions and/or increase the suspicion of a diagnosis of Reiter's syndrome.

For example, a blood rheumatoid factor (RF) test will generally be positive in rheumatoid arthritis, which has some similar symptoms, but generally negative in Reiter's syndrome. Other tests may include a C-reactive protein or erythrocyte sedimentation rate, which indicate an inflammatory process occurring somewhere in the body. A chlamydia test can diagnose the presence of a chlamydia infection, one of the infections that can lead to Reiter's syndrome. A test may also be run to check for the genetic factor HLA-B27, which increases the risk of developing Reiter's syndrome. X-rays may show some changes that are characteristic of Reiter's syndrome and may rule-out some other possible causes of symptoms.

It is possible that a diagnosis of Reiter's syndrome can be missed or delayed because symptoms can vary amongst individuals and can come and go. In addition, some symptoms may be similar to symptoms of other diseases and conditions. For more information on diseases and conditions that can mimic Reiter's syndrome, refer to misdiagnosis of Reiter's syndrome.

Treatment for Reiter's syndrome varies depending on the underlying infection, the severity of symptoms, the presence of complications, a person's age and medical history, and other factors. Reiter's syndrome cannot be cured, but treatment can help to reduce symptoms until the disorder resolves spontaneously on its own. Most people with Reiter's syndrome have a good long-term prognosis and symptoms disappear within about a year.

Treatment:

Treatment of Reiter's syndrome varies depending on the type of symptoms, the severity, and other factors. Treatment includes a multifaceted plan that addresses the symptoms and treats any underlying infection, such as chlamydia.

Reiter's syndrome cannot be cured, but treatment can minimize symptoms until the disorder resolves spontaneously on its own. Most people with Reiter's syndrome have a good long-term prognosis and symptoms disappear within about a year.

Commonly used medications for treatment of the pain and inflammation of Reiter's syndrome include acetaminophen and non-steroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen (Advil) and aspirin. These medications can have serious side effects and should only be taken as recommended by a physician. Corticosteroids may also be used to reduce inflammation. If bacterial conjunctivitis occurs, it is treated with antibiotic eye drops.

Physical therapy is also often recommended for Reiter's syndrome. Physical therapy includes exercises that can help to strengthen joints, relieve pain, and maintain flexibility and mobility.

septic arthritis

What is septic arthritis?

Septic, or infectious, arthritis is infection of one or more joints by microorganisms. Normally, the joint is lubricated with a small amount of fluid that is referred to as synovial fluid or joint fluid. The normal joint fluid is sterile and, if removed and cultured in the laboratory, no microbes will be found. With septic arthritis, microbes are identifiable in an affected joint fluid.

Most commonly, septic arthritis affects a single joint, but occasionally more joints are involved. The joints affected vary somewhat depending on the microbe causing the infection and the predisposing risk factors of the person affected. Septic arthritis is also called infectious arthritis.

What microbes cause septic arthritis?

Septic arthritis can be caused by bacteria, viruses, and fungi. The most common causes of septic arthritis are bacteria, including Staphylococcus aureus and Haemophilus influenzae. In certain "high-risk" individuals, other bacteria may cause septic arthritis, such as E. coli and Pseudomonas spp. in intravenous drug abusers and the elderly, Neisseria gonorrhoeae in sexually active young adults, and Salmonella spp. in young children or in people with sickle cell disease. Other bacteria that can cause septic arthritis include Mycobacterium tuberculosis and the spirochete bacterium that causes Lyme disease.

Viruses that can cause septic arthritis include hepatitis A, B, and C, parvovirus B19, herpes viruses, HIV (AIDS virus), HTLV-1, adenovirus, coxsackie viruses, mumps, and ebola. Fungi that can cause septic arthritis include histoplasma, coccidiomyces, and blastomyces.

Who's at Risk for Septic Arthritis?

Young children and elderly adults are most likely to develop septic arthritis. People with open wounds are also at a higher risk for septic arthritis. In addition, people with a weakened immune system and those with pre-existing conditions such as cancer, diabetes, intravenous drug abuse, and rheumatic and immune deficiency disorders have a higher risk of septic arthritis.

What Are the Symptoms of Septic Arthritis?

Symptoms of septic arthritis usually come on rapidly with intense pain, joint swelling, and fever. Septic arthritis symptoms may include:

• chills
• fatigue and generalized weakness
• fever
• inability to move the limb with the infected joint
• severe pain in the affected joint, especially with movement
• swelling (increased fluid within the joint)
• warmth (the joint is red and warm to touch because of increased blood flow)

How Is Septic Arthritis Diagnosed?

A procedure called arthrocentesis is commonly used to make an accurate diagnosis of septic arthritis. This procedure involves a surgical puncture of the joint to draw a sample of the joint fluid, known as synovial fluid. Normally, this fluid is sterile and acts as a lubricant.

In arthrocentesis, a needle is inserted into the affected joint. Fluid from the joint is collected in the needle and sent to a lab for evaluation. The lab compares the white blood cell count with normal synovial fluid, and watches the fluid for any bacterial growth. This will help the doctor determine if an infection is present, and which organism is causing it.

X-rays, MRIs, and blood tests can also be used to monitor inflammation. MRI scanning is sensitive in evaluating joint destruction. Blood tests can also be taken to detect and monitor inflammation.

What's the Treatment for Septic Arthritis?

Septic arthritis treatments include using a combination of powerful antibiotics as well as draining the infected synovial fluid from the joint. It's likely that antibiotics will be administered immediately to avoid the spread of the infection. Intravenous (IV) antibiotics may be given, which requires admission to the hospital.

Initially, empiric antibiotics are chosen to cover a wide range of infections. If the bacteria can be identified, antibiotics specific to that organism are used. It may take four to six weeks of treatment with antibiotics to ensure complete eradication of the infectious agents.

Is the Infected Fluid Drained?

Yes. Drainage of the infected area is critical for rapid clearing of the infection. Drainage is performed by removing the fluid with a needle and syringe. Often the draining occurs daily or with multiple surgical procedures. The exact method depends on the location of the joint. Warm compresses on the joint, elevation of the limb, and bed rest may be necessary.

Using arthroscopy, your doctor can irrigate the joint and remove the infected tissue. If drainage cannot be accomplished with joint aspirations or arthroscopy, open joint surgery is often necessary to drain the joint. If the fluid buildup is significant, the drains are left in place to remove excess fluid that may build up after the surgery.

juvenile idiopathic arthritis

Arthritis is a condition that affects the joints. It means one or more of your joints are swollen, painful and stiff (inflamed). Juvenile means the arthritis affects children under 16 years. Idiopathic means the cause is unknown. JIA affects about one in 1,000 children in the UK.

JIA is a chronic condition. A chronic illness is one that lasts a long time, sometimes for the rest of the affected person's life. When describing an illness, the term chronic refers to how long a person has it, not to how serious a condition is.

Types of juvenile idiopathic arthritis

There are three main types of JIA.

• Oligoarticular (or pauciarticular) JIA - the most common type, affecting only a few joints, usually the knees, ankles, elbows or wrists.
• Polyarticular JIA - the second most common type, affecting many joints including fingers and toes.
• Systemic JIA (Stills disease) - the rarest type where joint pain is part of a more general illness.

Symptoms of juvenile idiopathic arthritis

JIA affects all children differently. Symptoms may come and go over time with periods when they flare up and are worse. There may be times when your child has no symptoms at all - this is called remission.

The main symptoms of JIA are swollen, painful and stiff joints. The joint areas may look red and feel hot when you touch them. The exact symptoms and number of joints affected will vary depending on which type of JIA your child has.

Children with polyarticular JIA will have at least five or more joints affected including fingers and toes. Swelling and pain may also occur in hips, neck and jaw. Your child may also have other symptoms such as:

• nodules on their elbows
• a rash
• a fever

As well as joint pain, children with systemic JIA may have:

• a fever
• a rash
• swollen glands
• tiredness and lack of energy
• weight loss

Complications of juvenile idiopathic arthritis

JIA may affect your child's general growth. It's possible that your child's affected limbs may develop at different rates. For example if the arthritis is particularly bad in one knee the affected leg may be slightly shorter.

Anaemia may also be a problem. Anaemia is when there are too few red blood cells or not enough haemoglobin in the blood.

There is also a risk that your child may develop inflammation of the eyes (uveitis). Make sure your child has regular eye checks with an ophthalmologist (a doctor who specialises in eye health), even if he or she doesn't have any obvious symptoms.

There is a risk that systemic JIA may affect internal organs such as the tissue that covers the heart, liver or spleen. Children with systemic JIA may need to have regular check-ups.

Causes of juvenile idiopathic arthritis

The cause of JIA isn't fully understood at present but it's thought to be an autoimmune disease. An autoimmune disease is a condition caused by antibodies from the immune system attacking the body. It's possible that the tendency to develop the condition is inherited. However, it's thought that other factors are likely to be involved which are responsible for setting off this reaction of your child's immune system.

Diagnosis of juvenile idiopathic arthritis

Your GP will ask about your child's symptoms and examine him or her. Your GP may also ask you about your child's medical history.

There is no single test that can diagnose JIA and your GP will want to rule out other conditions that may be causing your child's symptoms. Your GP will usually refer your child to a paediatrician (a doctor who specialises in children's health).

Your child may need to have several tests, such as:

• blood tests to check haemoglobin levels and autoantibodies.
• X-rays, MRI, CT or ultrasound scan to check for any signs of inflammation in the joints or fluid build-up around the heart or lungs

Treatment of juvenile idiopathic arthritis

There isn't a complete cure for JIA, but there are treatments available to help control or ease the symptoms.

Your child will receive treatment from a team of health professionals. He or she will need regular check-ups to monitor his or her condition.

Self-help

Regular exercise such as swimming, running or aerobics may be helpful.

Your child will be given exercises by a physiotherapist to do at home. These will aim to reduce the pain and stiffness in your child's joints. Your child will need to do these exercises every day, even though he or she may not feel like it.

Using heat treatments, such as a hot water bottle wrapped in a towel may help to ease painful and swollen joints. A cold compress, such as ice or a bag of frozen peas, wrapped in a towel may also help. Never apply ice directly to your skin as it can give you an 'ice burn' - always place a cloth between the ice and skin.

Medicines

There are many different medicines available to help control symptoms, slow down or even stop the progression of JIA.

• Non-steroidal anti-inflammatory drugs (NSAIDs) - such as ibuprofen, can help ease pain, stiffness and swelling. For some children with mild JIA, this may be the only medicine they need to take.
• Painkillers - such as paracetamol can help ease joint pain.
• Steroids - such as prednisolone can help ease swelling. Steriods may be given as tablets, injection into a tissue or joint or through a drip into a vein.
• Disease-modifying antirheumatic drugs (DMARDs) - such as methotrexate can ease swelling and slow down the disease process. Most importantly, by controlling arthritis they can help reduce how much steroids your child needs to keep well. It may take up to three months for these medicines to have an effect.
• Etanercept is a new type of medicine and it works by blocking the action of a part of the immune system. Your child may be offered this medicine if other medicines haven't helped.

Raynaud's phenomenon

What is Raynaud's phenomenon?

Raynaud's phenomenon (RP) is a condition resulting in a particular series of discolorations of the fingers and/or the toes after exposure to changes in temperature (cold or hot) or emotional events. Skin discoloration occurs because an abnormal spasm of the blood vessels causes a diminished blood supply to the local tissues. Initially, the digit(s) involved turn white because of the diminished blood supply. The digit(s) then turn blue because of prolonged lack of oxygen. Finally, the blood vessels reopen, causing a local "flushing" phenomenon, which turns the digit(s) red. This three-phase color sequence (white to blue to red), most often upon exposure to cold temperature, is characteristic of RP.

What causes Raynaud's phenomenon?

The causes of primary and secondary RP are unknown. Both abnormal nerve control of the blood-vessel diameter and nerve sensitivity to cold exposure have been suspected as being contributing factors. The characteristic color changes of the digits are in part related to initial blood-vessel narrowing due to spasm of the tiny muscles in the wall of the vessels, followed by sudden opening (dilation), as described above. The small arteries of the digits can have microscopic thickness of their inner lining, which also leads to abnormal narrowing of the blood

What conditions have been associated with Raynaud's phenomenon?

Raynaud's phenomenon has been seen with a number of conditions, including rheumatic diseases (scleroderma, rheumatoid arthritis, systemic lupus erythematosus), hormone imbalance (hypothyroidism and carcinoid), trauma (frostbite, vibrating tools), medications (propranolol [Inderal], estrogens without additional progesterone, bleomycin [Bleoxane] used in cancer treatment, and ergotamine used for headaches), nicotine, and even rarely with cancers.

A typical Raynaud’s phenomenon attack may go something like this: You are fixing dinner and go into the freezer to get a bag of peas. They are buried in the back and you have to move things around for a moment before you find them. By the time you close the freezer door, your fingers turn white and they feel cold, numb and start to hurt. The fingers then turn blue. After 10 minutes or so they turn red, tingle, throb and get warm again.

So, the symptoms of Raynaud’s phenomenon are:

• Extreme sensitivity to cold

• Body reacts to emotional stress as if it were reacting to cold

• Skin color changes: Fingers and/or toes (and sometimes ears, lips, nose) turn white due to lack of blood flow (called pallor). The blood that’s left in the tissues loses its oxygen and the fingers turn blue (called cyanosis). Finally, the skin will turn red (called rubor) as fresh oxygenated blood returns to the fingers once the vessels open.

• Coldness, pain and numbness: A lack of oxygenated blood in the fingers triggers feelings of coldness, pain and numbness – the sensation that the hands fingers have fallen asleep.

• Warmth, tingling and throbbing: The quick return of blood to the fingers triggers feelings of warmth, tingling and throbbing, like when your hands “wake up” again.

• Skin ulcers: If your Raynaud’s phenomenon is severe and your attacks tend to last a long time, you may get painful, slow-healing sores on the tips of your fingers.

• Gangrene: In rare cases, a long-term lack of oxygen to the tissues can result in gangrene and amputation of the affected digit.

Diagnosis:

Your primary care doctor can usually determine if you have Raynaud’s phenomenon simply by listening to you describe an attack. You may even have an attack while at the doctor’s office. Determining whether the disorder is primary or secondary to an underlying disease may take some time and testing, however.

To determine whether your Raynaud’s is primary or secondary, your doctor may

• Look at the nailfold capillaries. To do this, the doctor may place a drop of oil on your skin at the base of your fingernail; you will then hold your finger under a microscope. If the capillaries are enlarged or deformed, you may have a connective tissue disease.

• Send your blood to the lab. If you have antinuclear antibodies in your blood, you may have a connective tissue disease or other autoimmune disorder. If you have an elevated erythrocyte sedimentation rate, you may have an inflammatory disorder.

• Perform tests of the blood vessels to see if there is blockage of blood flow in the arms or legs. This is often done with ultrasound, or sometimes with x-rays and dye (angiogram).

Criteria for the diagnosis of Raynaud’s phenomenon:

• Primary Raynaud’s Phenomenon
  • Periodic vasospastic attacks of pallor or cyanosis (some doctors add that the attacks should have been present for at least two years)
  • Normal nailfold capillary pattern
  • Negative antinuclear antibody test
  • Normal erythrocyte sedimentation rate
  • Absence of pitting scars or ulcers of the skin, or gangrene (tissue death) in the fingers or toes

• Secondary Raynaud’s Phenomenon
  • Periodic vasospastic attacks of pallor and cyanosis
  • Abnormal nailfold capillary pattern
  • Positive antinuclear antibody test
  • Abnormal erythrocyte sedimentation rate
  • Presence of pitting scars or ulcers of the skin, or gangrene in the fingers or toes

Treatment option:

For most people with Raynaud’s phenomenon, a conservative approach not using medicines is sufficient to control attacks. For people with more severe attacks, medications can be added.

To shorten the length of an attack once it has started, try these tips:

• Warm your hands or feet in warm (not hot) water.
• Swing your arms in large circles to increase circulation.

• Use relaxation techniques, such as deep breathing or meditation.

• Practice biofeedback methods.

Self-help treatments for preventing attacks include:

• Dress warmly: It is important not only to keep your hands and feet warm, but you also must keep your whole body warm.
  • Wear layers of loose-fitting clothing, warm socks, hats, scarves and gloves or mittens in cold weather. Mittens are warmer than gloves because they trap more air and let the fingers warm each other.
  • Keep a sweater or jacket with you at all times, even in the summer. You may need it in cold, air-conditioned buildings.

• Control your body temperature at home.

• Use flannel sheets or layers of blankets. Use an electric blanket to warm the sheets before you get into bed (make sure you follow the user instructions carefully). Consider wearing mittens and socks to bed if your hands and feet get cold when you sleep.
• Keep the rooms you use most often at a comfortable temperature.
• Start running your bath or shower water before you are ready to bathe so you don’t touch cold water. Keep the bathroom door closed so the steam will warm the room.
• Avoid cold items. Use insulated drinking glasses for your cold drinks; wear gloves when reaching in the freezer; use tepid water to rinse vegetables or hand-wash clothing.
• Use chemical warmers. Small heating pouches can be placed in your pockets, mittens or boots when you need to be outside in the cold for a while.

• Protect your skin: Poor blood flow may make your skin dry. It also may cause cuts, cracks or sores to heal more slowly than usual.
  • Use lotion with lanolin every day on your hands and feet to keep your skin from chapping or cracking.
  • Wash with a mild, creamy soap. Clean between your fingers and toes, but don’t soak them.
  • Examine your feet and hands daily to check for ulcers. If you develop one, keep it clean and covered. See your doctor right away.
  • Protect your nails. Use lotion to keep your cuticles soft. Carefully cut hangnails and file your nails in a rounded fashion to the tips of your fingers.

• Quit smoking: Chemicals in cigarette smoke constrict blood vessels – something you definitely don’t need if you have Raynaud’s phenomenon.

• Control stress: Stress and emotional upset can trigger a Raynaud’s attack, so avoiding stressful situations and learning to relax once you’re feeling anxious can lessen the number of attacks you have. Relaxation techniques and biofeedback training can be learned through a stress management program.

Medical treatments to control severe Raynaud’s phenomenon include:

• Calcium-channel blockers and alpha blockers: These drugs (such as nifedipine [Procardia] and doxazosin [Cardura]) relax smooth muscle and dilate small blood vessels. They decrease the frequency and severity of attacks and help skin ulcers heal.

• Nitroglycerine paste: This vasodilator (a drug that dilates blood vessels) can be applied to the fingers to help heal skin ulcers.

• Antibiotic ointment: In some cases needed to prevent ulcers from becoming infected.

• Analgesics: Pain-relieving drugs, sometimes containing narcotics, may be needed to control the pain of skin ulcers.

• Prostaglandin and prostacyclin: Intravenous prostaglandin and prostacyclin may be needed for some people with severely affected digits.

• Arm pump: A counterpulsation arm pump which keeps blood in the arm at higher pressures is available and may be helpful in managing ulcers of the fingers resulting from severe Raynaud’s phenomenon.

• Surgery: In severe cases, a doctor may recommend surgery to treat Raynaud’s phenomenon. Surgical procedures that are used to treat Raynaud’s phenomenon include cutting the nerves that cause narrowing of the blood vessels or performing vascular surgery to widen the blood vessels causing the Raynaud’s phenomenon. These procedures are done mainly for very severe secondary forms of the condition.