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I.

DESCRIPTION & DEFINITION

Gout is a painful condition that occurs when the bodily waste product uric acid is deposited as needle-like crystals in the joints and/or soft tissues. In the joints, these uric acid crystals cause inflammatory arthritis, which in turn leads to intermittent swelling, redness, heat, pain, and stiffness in the joints. II. ETIOLOGY

Risk Factors: *Predisposing/Modifiable a) Weight. Being overweight increases the risk of developing hyperuricemia and gout because there is more tissue available for turnover or breakdown, which leads to excess uric acid production. b) Alcohol consumption. Drinking too much alcohol can lead to hyperuricemia, because alcohol interferes with the removal of uric acid from the body. c) Diet. Higher levels of consumption of meat (especially organ meats such as liver, kidney, and brain and as well as meat extracts and gravies), dried beans and peas, sardines, anchovies, and seafood are associated with an increased risk of gout. Also, a higher level of consumption of dairy products is associated with a decreased risk of gout. d) Lead exposure. In some cases, exposure to lead in the environment can cause gout. e) Medications. A number of medications may put people at risk for developing hyperuricemia and gout. They include: 1)diuretics, such as furosemide (Lasix*), hydrochlorothiazide (Esidrix, Hydro-chlor), and metolazone (Diulo, Zaroxolyn), which are taken to eliminate excess fluid from the body in conditions like hypertension, edema, and heart disease, and which decrease the amount of uric acid passed in the urine. 2)salicylate-containing drugs, such as aspirin. 3)niacin, a vitamin also known as nicotinic acid. 4)cyclosporine (Sandimmune, Neoral), a medication that suppresses the bodys immune system (the system that protects the body from infection and disease). This medication is used in the treatment of some autoimmune diseases, and to prevent the bodys rejection of transplanted organs. 5)levodopa (Larodopa), a medicine used to support communication along nerve pathways in the treatment of Parkinsons disease. *Precipitating/Non-modifiable a) Family history of gout. If other members of your family have had gout, you're more likely to develop the disease. b) Age and sex. Gout occurs more often in men than it does in women, primarily because women tend to have lower uric acid levels than men do. After menopause, however, women's uric acid levels approach those of men. Men also are more likely to develop gout earlier usually between the ages of 40 and 50 whereas women generally develop signs and symptoms after menopause. c) Medical conditions. Certain diseases and conditions make it more likely that you'll develop gout. These include untreated high blood pressure (hypertension) and chronic conditions, such as diabetes, high levels of fat and cholesterol in the blood (hyperlipidemia), and narrowing of the arteries (arteriosclerosis).

*Prevalence and Incidence According to the National Health and Nutrition Examination Survey III, 1988-1994, an estimated 5.1 million people in the United States suffer from gout. According to the National Institutes of Health (NIH), gout accounts for about 5% of all cases of arthritis reported in the United States. Gout is the most common form of inflammatory arthritis in men. Gout affects approximately 3 times as many men as women, and men are more likely than women to have gout at all ages. Racial and ethnic differences are not as distinct among patients in the US, though African Americans aged 45 years or older are more likely to have gout than Caucasians in the same age group. Some worldwide prevalence observations:

Black Africans, Japanese, and Native Americans have generally lower levels than Caucasian populations. Compared to other populations, higher urate levels are found in adult ethnic men in Oceania. Ethnic groups in Malaysia and China have higher mean urate levels than most Caucasian populations.

In one longitudinal study, the cumulative incidence of all gout was 8.6% among men, with a median age at study entry of 22 years and a median follow-up of 29 years. In general, gout has an annual incidence of 1 to 3 per 1000 men. The rate in all women is approximately 1 in 5000; however, the incidence of gout in women increases after menopause. There is also some evidence that the prevalence and incidence of gout appear to be rising. Multiple studies over the last 40 years have provided data consistent with a considerable increase in prevalence and annual incidence in Westernized industrial countries. Gout appears to be on the increase in the American population. According to a study published in November 2002, there was a twofold increase in the incidence of gout over the 20 years between 1977 and 1997. It is not yet known whether this increase is the result of improved diagnosis or whether it is associated with risk factors that have not yet been identified. III. SIGNS & SYMPTOMS

Symptoms 1. Associated Symptoms 1. Chills 2. Fever as high as 104 F (40 C) 2. Severity: Very severe pain 1. Unable to bear weight 2. Too painful to put on socks 3. Intollerant to light touch from blankets 3. Region: 1. First Metatarsophalangeal joint of great toe (most common) 1. Known as Podagra 2. Affected in 50% of first gout attacks 2. Mid-tarsal joints 3. Ankle joints 4. Knee joints

4. Characteristics: Joint pain 1. Excruciating, crushing type pain 5. Timing: Joint pain 1. Acute onset of lower extremity joint pain 2. Wakens patient from sleep Signs 1. Acute 1. Joint Inflammation 1. Erythema, tenderness and swelling at affected joint 2. Pain extends well beyond joint 1. Entire foot involved in some cases 3. Asymmetric joint involvement 1. May only involve one side with the first attack 2. Skin over joint is tense and shiny 2. Chronic 1. Gouty Tophi (develop after >=10 years) 2. Chronic arthritis 1. Chronic deposition occurs with recurrent attacks Complications People with gout can develop more-severe conditions, such as:

Recurrent gout. Some people may never experience gout signs and symptoms again. But others may experience gout several times each year. Medications may help prevent gout attacks in people with recurrent gout. Advanced gout. Untreated gout may cause deposits of urate crystals to form under the skin in nodules called tophi (TOE-fi). Tophi usually aren't painful, but they can become swollen and tender during gout attacks. Kidney stones. Urate crystals may collect in the urinary tract of people with gout, causing kidney stones. Medications can help reduce the risk of kidney stones.

IV.

ANATOMY AND PHYSIOLOGY

Your foot is made up of 3 sections. Your forefoot is comprised of 4 smaller toes (phalanges) and 1 big toe (hallux). Your midfoot (metatarsal bones) and hindfoot (tarsal bones) make up your foot arches, instep, heel and ankle; these are responsible for weight bearing and propulsion. Your arches contain bones, ligaments, muscles and tendons of your foot, which require a lot of stability and flexibility. Your foot bones work with your foot muscles to move your foot in 4 directions: dorsiflexion (moving foot upward), plantar flexion (moving foot downward towards sole), abduction (moving foot outward) and adduction (moving foot inward). Your lower leg muscles have long tendons that cross your ankle and attach to your foot and toe bones to help move your foot. Your extensor muscles and tendons attach on the top of your foot, and your flexor, abductor and adductor muscles and tendons attach on the bottom of your foot. Your achilles tendon is the strongest and largest tendon in your body and it connects your calf muscles (gastrocnemius and soleus) to your heel bone (calcaneus), allowing your foot to push off when your calf muscles tighten. It is essential for walking, running and jumping.

V.

PATHOPHYSIOLOGY

In gout, excess uric acid causes needle-shaped crystals to form in the synovial fluid. Uric acid is a normal chemical in the blood that comes from the breakdown of other chemicals in the body tissues. As the immune system tries to get rid of the crystals, inflammation develops. The inflammatory process in the synovial space and joint fluid causes symptoms of joint pain and swelling. This is the result of polymorphonuclear cells activating the release of prostaglandins and leukotrienes, with the generation of reactive oxygen species. The destruction of cartilage and bone is caused by activated lymphocytes and monocytes that release inflammatory proteinases and prostanoids. For the person with too much uric acid, this inflammation can cause painful arthritis. The first attack of gouty arthritis usually happens in just one joint. Half of the time, gout affects the metatarsophalangeal (MTP) joint.

VI. Labs

LABORATORIES AND DIAGNOSTIC TESTS

1. Complete Blood Count 1. Leukocytosis (may be as high as 40,000 wbc/mm3) 2. Serum Uric Acid increased (Hyperuricemia) 1. Synovial Fluid Exam (critical if Septic Arthritis is considered) 2. Polarizing Microscopy 1. Negatively birefringent 2. Needle shaped Uric Acid crystals 3. Gram Stain and Culture 1. Rule out Septic Arthritis 3. Urine Uric Acid (24 hour collection) Imaging: Affected joint(s) 1. X-ray of affected joint shows asymmetric swelling VII. MEDICAL & SURGICAL MANAGEMENT

*Medical Management (with Drug Study on separate sheet) Anti-Gout Meds: 1) 2) 3) 4) 5) Allopurinol Colchicine Indomethacin Probenecid Sulfinpyrazone

Acute Treatment: - NSAIDS: indomethacin - colchicine: prophylactic administration may reduce frequency of multiple attacks; - steroids may be indicated if NSAIDS and colchicine cannot be given; - contra-indicated medications: allopurinol and probenecid may worsen symptoms during acute attack; - these medications may cause precipitation of urate if given during the acute attack; Recurrent Attacks: - requires reduction of miscible pool of urate; - goal is to reducing serum urate concentrations to less than 6.0 mg /dl (360 mol / lit); - if trophi are present, then uric acid level needs to be lower than 5.0 mg / dl (300 mol per liter) - need to determine whether pt w/ recurrent gouty episodes is: - over producer (10% of primary gout); - allopurinol (xanthine oxidase inhibitor) is indicated in patients with increased urate production - uricosuric drugs (probenecid) are contraindicated in these type patients; - underexcreter of uric acid (90% primary gout) or .... - treated with probenecid, sulfinpyrazone, or allopurinol; - for pts w/ normal urinary urate excretion, then use probenecid; - blocks renal resorption of uric acid, thus increasing net excretion; - probencid is contraindicated for pts w/ history of renal stones or elevated urinary urate excretion rates; - alternatively, allopurinol is also effective for these patients as well; Chronic Gout: - Allopurinol

- administered on long-term basis to pts w/ gout to block purine degradation; - inhibits xanthine oxidase which increases blood levels of xanthine and hypoxanthine which are excreted in urine; * Surgical management Surgery is rarely needed for gout unless significant joint damage has occurred from lack of effective treatment. VIII. NURSING MANAGEMENT

Nursing Diagnosis with Management PAIN related to joint inflammation, traction, surgical intervention 1. Assess patients perception of pain 2. Instruct patient alternative pain management like meditation, heat and cold application, TENS and guided imagery 3. Administer analgesics as prescribed:Usually NSAIDS, Meperidine can be given for severe pain 4. Assess the effectiveness of pain measures IMPAIRED PHYSICAL MOBILITY 1. Instruct patient to perform range of motion exercises, either passive or active 2. Provide support in ambulation with assistive devices 3. Turn and change position every 2 hours 4. Encourage mobility for a short period and provide positive reinforcements for small accomplishments SELF-CARE DEFICITS 1. Assess functional levels of the patient 2. Provide support for feeding problems Place patient in Fowlers position Provide assistive device and supervise mealtime Offer finger foods that can be handled by patient Keep suction equipment ready

3. Assist patient with difficulty bathing and hygiene Assist with bath only when patient has difficulty Provide ample time for patient to finish activity

Nursing Intervention for Gouty Arthritis 1. Provide a diet with LOW purine

Avoid Organ meats, aged and processed foods STRICT dietary restriction is NOT necessary

2. Encourage an increased fluid intake (2-3L/day) to prevent stone formation 3. Instruct the patient to avoid alcohol 4. Provide alkaline ash diet to increase urinary pH 5. Provide bed rest during early attack of gout 6. Position the affected extremity in mild flexion 7. Administer anti-gout medication and analgesics

Sources: http://www.gout.com/professional/gout_information/prevalence_and_incidence.aspx http://www.mayoclinic.com/print/gout/DS00090/DSECTION=all&METHOD=print http://www.niams.nih.gov/Health_Info/Gout/default.asp http://www.aidmygout.com/gouty-arthritis.php altmed.creighton.edu/.../rheumatoidoverview.htm www.eorthopod.com/.../6588/gout.html www.mahonkin.com/~milktree/gout/gout.html http://www.fpnotebook.com/Rheum/Joint/GtyArthrts.htm http://www.emedicinehealth.com/gout/article_em.htm#Gout%20Overview http://www.nlm.nih.gov/medlineplus/gout.html#cat1 http://www.wheelessonline.com/ortho/management_of_gout http://philippinenurses.blogspot.com/2007/11/musculoskeletal-system-medical-surgical.html