I.

DESCRIPTION & DEFINITION Gout is a painful condition that occurs when the bodily waste product uric acid isdeposited as needle-like crystals in the joints and/or soft tissues. In the joints, theseuric acid crystals cause inflammatory arthritis, which in turn leads to intermittentswelling, redness, heat, pain, and stiffness in the joints. II.ETIOLOGY Risk Factors:*Predisposing/Modifiable a) Weight. Being overweight increases the risk of developing hyperuricemia andgout because there is more tissue available for turnover or breakdown, whichleads 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 andpeas, sardines, anchovies, and seafood are associated with an increased risk of gout. Also, a higher level of consumption of dairy products is associated with adecreased risk of gout. d) Lead exposure. In some cases, exposure to lead in the environment can causegout. e) Medications. A number of medications may put people at risk for developinghyperuricemia 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 likehypertension, edema, and heart disease, and which decrease the amount of uricacid passed in the urine. 2)salicylate-containing drugs, such as aspirin. 3)niacin,a vitamin also known as nicotinic

acid. 4)cyclosporine (Sandimmune, Neoral), amedication that suppresses the bodys immune system (the system that protectsthe body from infection and disease). This medication is used in the treatment of some autoimmune diseases, and to prevent the bodys rejection of transplantedorgans. 5)levodopa (Larodopa), a medicine used to support communicationalong 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'remore likely to develop the disease. b) Age and sex. Gout occurs more often in men than it does in women, primarilybecause women tend to have lower uric acid levels than men do. After menopause, however, women's uric acid levels approach those of men. Menalso are more likely to develop gout earlier usually between the ages of 40and 50 whereas women generally develop signs and symptoms after menopause. c) Medical conditions. Certain diseases and conditions make it more likely thatyou'll develop gout. These include untreated high blood pressure(hypertension) and chronic conditions, such as diabetes, high levels of fat andcholesterol in the blood (hyperlipidemia), and narrowing of the arteries(arteriosclerosis).

*Prevalence and IncidenceAccording 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 tothe 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 affectsapproximately 3 times as many men as women, and men are more likely than women tohave gout at all ages. Racial and ethnic differences are not as distinct among patients inthe US, though African Americans aged 45 years or older are more likely to have goutthan Caucasians in the same age group.Some worldwide prevalence observations: Black Africans, Japanese, and Native Americans have generally lower levels thanCaucasian populations.

Compared to other populations, higher urate levels are found in adult ethnic menin Oceania. Ethnic groups in Malaysia and China have higher mean urate levels than mostCaucasian 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. Ingeneral, gout has an annual incidence of 1 to 3 per 1000 men. The rate in all women isapproximately 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 berising. Multiple studies over the last 40 years have provided data consistent with aconsiderable increase in prevalence and annual incidence in Westernized industrialcountries.Gout appears to be on the increase in the American population. According to a studypublished in November 2002, there was atwofoldincrease in the incidence of gout over the 20 years between 1977 and 1997. It is not yet known whether this increase is theresult of improved diagnosis or whether it is associated with risk factors that have notyet been identified. III.SIGNS & SYMPTOMS Symptoms1.Associated Symptoms1.Chills 2. Fever as high as 104 F (40 C)2.Severity: Very severe pain1.Unable to bear weight2.Too painful to put on socks3.Intollerant to light touch from blankets 3. Region:1.First Metatarsophalangeal joint of great toe (most common)1.Known as Podagra2.Affected in 50% of first gout attacks2.Mid-tarsal joints3.Ankle joints4.Knee joints

4.Characteristics: Joint pain1.Excruciating, crushing type pain5.Timing: Joint pain1.Acute onset of lower extremity joint pain2.Wakens patient from sleepSigns1.Acute1.Joint Inflammation1.Erythema, tenderness and swelling at affected joint2.Pain extends well beyond joint1.Entire foot involved in some cases3.Asymmetric joint involvement1.May only involve one side with the first attack 2. Skin over joint is tense and shiny2.Chronic

1. Gouty Tophi(develop after >=10 years)2.Chronic arthritis1.Chronic deposition occurs with recurrent attacksComplicationsPeople with gout can develop more-severe conditions, such as: Recurrent gout. Some people may never experience gout signs and symptomsagain. But others may experience gout several times each year. Medications mayhelp prevent gout attacks in people with recurrent gout. Advanced gout. Untreated gout may cause deposits of urate crystals to formunder the skin in nodules called tophi (TOE-fi). Tophi usually aren't painful, butthey 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. ANATOMYANDPHYSIOLOGY 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 (tarsalbones) make up your foot arches, instep, heel and ankle; these are responsible for weight bearing and propulsion. Your arches contain bones, ligaments, muscles andtendons 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 legmuscles have long tendons that cross your ankle and attach to your foot and toe bonesto 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 bottomof your foot. Your achilles tendon is the strongest and largest tendon in your body and itconnects 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 jointfluid 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 andbone is caused by activated lymphocytes and monocytes that release inflammatoryproteinases and prostanoids.For the person with toomuch uric acid, thisinflammation can causepainful arthritis. The firstattack of gouty arthritisusually happens in justone joint. Half of the time,gout affects the metatarsophalangeal (MTP) joint

VI.LABORATORIES AND DIAGNOSTIC TESTS Labs

1. Complete Blood Count 1. Leukocytosis(may be as high as 40,000 wbc/mm3) 2. SerumUric Acidincreased (Hyperuricemia) 1. Synovial FluidExam (critical if Septic Arthritisis considered) 2 . P o l a r i z i n g Microscopy1.Negatively birefringent 2. Needle shapedUric Acidcrystals 3. Gram Stainand Culture 1. Rule outSeptic Arthritis 3. Urine Uric Acid(24 hour collection)Imaging: Affected joint(s) 1. X-ray of affected joint shows asymmetric swellingV I I . M E D I C A L & S U R G I C A L M A N A G E M E N T *Medical Management ( with Drug Study on separate sheet) Anti-Gout Meds: 1) Allopurinol 2)

Colchicine 3) Indomethacin 4) Probenecid5 ) S u l f i n p y r a z o n e Acute Treatment:-NSAIDS:indomethacin -colchicine:prophylactic administration may reduce frequency of multiple attacks;-steroidsmay be indicated if NSAIDS and colchicine cannot be given;- contra-indicated medications:allopurinolandprobenecidmay worsen symptoms during acute attack;- these medications may cause precipitation of urate if given during the acuteattack;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 (300mol 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 increasedurate production- uricosuric drugs (probenecid) are contraindicated in these type patients;- underexcreter of uric acid(90% primary gout) or ....treated withprobenecid, sulfinpyrazone, or allopurinol; - for pts w/ normal urinary urate excretion, then useprobenecid;- 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 andhypoxanthine which are excreted in urine;* Surgical managementSurgery is rarely needed for gout unless significant joint damage has occurred from lackof effective treatment. VIII.NURSING MANAGEMENT Nursing Diagnosis with ManagementPAIN related to joint inflammation, traction, surgical intervention1. Assess patients perception of pain2. Instruct patient alternative pain management like meditation, heat and coldapplication, TENS and guided imagery3. Administer analgesics as prescribed:Usually NSAIDS, Meperidine can be given for severe pain4. Assess the effectiveness of pain measuresIMPAIRED PHYSICAL MOBILITY1. Instruct patient to perform range of motion exercises, either passive or active2. Provide support in ambulation with assistive devices3. Turn and change position every 2 hours4. Encourage mobility for a short period and provide positive reinforcements for small accomplishmentsSELF-CARE DEFICITS1. Assess functional levels of the patient2. 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 ready3. Assist patient with difficulty bathing and hygiene Assist with bath only when patient has difficulty Provide ample time for patient to finish activityNursing Intervention for Gouty Arthritis1. 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 alcohol4. Provide alkaline ash diet to increase urinary pH 5. Provide bed rest during early attack of gout6. Position the affected extremity in mild flexion7. Administer antigout medication and analgesics
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