Gout is a prevalent and debilitating disease.  It is progressive in nature and it can be precipitated by many things.  It is similar to other arthritis diseases in that it involves inflammation, effects the joints, and causes severe pain.  Unlike osteoarthritis and some other forms of arthritis that are strictly localized to the joint, gout can affect the entire body, leaving the patient completely incapacitated and even hospitalized if not treated properly.  This paper will discuss Gout and is meant to be a guide for Nurse Practitioners to use in practice.

Definition, Pathophysiology, and Epidemiology

            Gout is defined as a type of arthritis because it involves an inflammation of the joints.  A definition by Vannucchi, 2012, is that it is “characterized by elevated serum uric acid (SUA) levels, inflammation, and urate crystal deposition in and around joints causing acute, intense pain” (p 191).  Gout has been around since the 18th century.  It was known to affect the rich man and was depicted in many cartoons as a demon gnawing relentlessly at ones joint (Harvard Health Letter, 2010).  Even the name is ancient.  Gout comes from the Latin word for drop, which came from the belief that “gout happened from drop by drop humors accumulating in the joints” (Harvard Health Letter, 2010, p3).  Rich men were often overweight and indulged in meat, alcohol, and seafood; even now this can be considered a disease of an overweight individual due to its pathophysiology.  The etiology is too much uric acid in the blood, but it is also linked to genetic factors.

As stated in the introduction, gout is a prevalent disease.  According to Hilaire and Wozniak, 2010, “an estimated 3 to 5 million [people] suffer and its prevalence appears to be increasing. Gout affects about 2% of men (>30 years) and women (>50 years)” (p 84).  Gout affects 2% of people, which is more than rheumatoid arthritis.  This disease does affect black men more often than other groups and this is most likely due to the large incidence of hypertension in this group (Dunphy, Winland-Brown, Porter, Thomas, 2011).  The risk factors include, hypertension, advanced age, male gender, postmenopausal women, high BMI, high alcohol intake, diet high in meat and seafood, and genetic influences (Hilaire & Wozniak, 2010).  Certain drugs such as low dose aspirin and diuretics can also contribute to an acute attack of gout.  The associated co-morbidities with hyperuricemia and gout are diabetes mellitus, hypertension, metabolic syndrome, obesity, cardiovascular disease, hyperlipidemia, and renal manifestations (Hilaire and Wozniak, 2010).

In 90% of cases of gout the cause is under excretion of uric acid not overproduction of it (10%).  Uric acid is the end product of catabolism of purines (Vannucchi, 2012).  Xanthine and hypoxanthine, a byproduct of purines catabolism, is broken down by xanthine oxidase to produce uric acid.  Uric acid is then excreted by the alimentary or urinary systems.  If there is excess uric acid, from eating a lot of meat, drinking a lot of alcohol, or poor kidney function, then uric acid in the form of monosodium urate crystals, gets deposited around the joints (Hilaire and Wozniak, 2010).  A bump or injury to the area can release the crystals into the joint space causing an acute exacerbation of gout.  Other things that can cause the crystals to be released is acute stress caused by surgery or infection.  There are four critical stages of gout.  The first stage is called the asymptomatic stage.  This stage is characterized by no symptoms or gout, but the uric acid level is usually greater than 6.5 mg/dL (Vannucchi, 2012).  No history of gout attacks has been recorded, but the deposition of urate has begun at this stage and these deposits can directly contribute to organ damage.  The next stage is an acute attack.  A traumatic event, such as an infection or trauma (even just stubbing a toe), will cause the crystals to dislodge and enter the joint space.  This involves acute inflammation and intense pain.  This is the phase where management needs to be optimized.  The intercritical stage is the time between gouty flare ups.  “When the crystal deposits continue to accumulate, patients develop stiff and swollen joints leading to the final phase, chronic advanced gout. This includes long-term complications of uncontrolled hyperuricemia such as chronic arthritis and tophi” (Hilaire and Wozniak, 2010).  Tophi are large nodules of crystals that have deposited in soft tissue.  This phase is uncommon because it can be avoided with proper management.  Refer to the management section for ways to properly prescribe medications for this disease.

Social Determinants

            The social determinants of this disease are age, race, and gender.  Black males between the ages of 40 and 50 will be the group that is most affected potentially because this group is largely affected by severe hypertension and kidney diseases (Dunphy, Windland-Brown, Porter, Thomas, 2011).  The prevalence of this disease is increasing and this is thought to be because of an increase in the use of diuretics and low dose aspirin, but also because there is a large group of people getting older, namely the baby boomers.  Another reason this disease may be becoming more prevalent is the greater amount of kidney disease and overweight individuals, which are both associated with gout.

Case Study

            Michael is a 53 year old African American male that presents with an excruciatingly painful, and hot index finger on his right hand.  He is in so much distress because he is right handed and works construction; He states, “I haven’t been able to work the past week because the pain has been so bad and it has only gotten worse.”  He states he tried taking ibuprofen and Tylenol, but they only relieve the pain for a short while.  He does not remember bumping his finger on anything or having any recent trauma but states that it is possible since he works construction.  He has also used ice on it and this has helped some.  “I have also felt feverish the past two days, I think I might be getting sick.”  When asked about drinking he admitted to drink a beer every night and does not have the “best diet.” 

Family history includes gout, diabetes mellitus type II, hypertension, coronary artery disease, and hyperlipidemia on his paternal side.  Hypertension on his maternal side.

Medical diagnoses include: hypertension, hyperlipidemia, and diabetes mellitus type II.  Medications include Hydrochlorothiazide/Lisinopril 25mg/40mg PO Daily, Metformin 500mg PO BID, aspirin 81mg Daily, and atorvastatin 40mg PO daily.

            Weight: 250lbs, Height: 5 foot 9 inches, BMI: 36.9, BP: 165/88, HR: 67, Temp: 99.2

On physical exam, a swollen and red middle interphalangeal joint of the index finger is noted.  Tenderness and heat upon palpation of this joint.  Limited range of motion in right hand, especially at the index finger.  Left hand has full range of motion with no redness, swelling, or tenderness. Diagnostic tests include: a serum uric acid level, BUN, creatinine, ESR, CBC (focusing on the WBC level), and an x-ray of the finger.  Serum uric acid level: 9.0 mg/dL; WBCs 12,000 10^6/L; Creatinine: 1.34 mg/dL, BUN: 38, and ESR is elevated.  The x-ray of the joint revealed “punched out” erosions of bone (Dunphy, Windland-Brown, Porter, Thomas, 2011).  Differential diagnoses include gout, Rheumatoid arthritis, osteoarthritis, fracture, or trauma (Mead, Arabindoo, & Smith, 2014). Fracture, osteoarthritis and trauma was ruled out with x-ray. Rheumatoid arthritis can be ruled out with history and presentation.

Management and Patient Education

            Due to the prevalence of gout, understanding how to manage it is a very important part of being a primary care provider.  Part of managing gout is understanding when and why flare-ups occur therefore keeping a complete record of flare-ups will be important (Mead, Arabindoo, & Smith, 2014).  In the asymptomatic phase there is no gout attack and the patient does not present with symptoms therefore there is no management.  The acute phase requires quick, usually within the first 24 hours of onset, and effective treatment at the first sign of the attack.  Most of the time the acute attack will occur in the joint of the big toe, often referred to as podgara (Dunphy, Windland-Brown, Porter, Thomas, 2011).  “For moderate pain involving a few small joints or one or 2 large joints, monotherapy with a nonsteroidal anti-inflammatory drug (NSAID), a corticosteroid, or colchicine is recommended.  For severe pain and/or polyarticular involvement (≥4 joints in more than one region of the body), combination therapy is recommended (eg, colchicine and either an NSAID or a corticosteroid).” (Mead, Arabindoo, & Smith, 2014).  Colchicine is a first line anti-gout medication that is given when the first symptom of a gout attack occurs and should not be given 36 hours after an attack starts.  Dosing is 1.2 mg loading dose, followed by 0.6mg every hour until resolution (do not exceed 1.8mg/day and do not repeat dosing for more than 3 days) (Mead, Arabindoo, & Smith, 2014).  Naproxen (250mg PO TID) or Indomethacin (50mg PO TID) can be used for NSAID therapy and should be given every eight hours for pain relief (Mead, Arabindoo, & Smith, 2014). 

            Chronic gout has a very different treatment.  The goal of therapy for chronic gout is to keep the uric acid level below 6.0 mg/dL (Mead, Arabindoo, & Smith, 2014).  There are several qualifying factors for chronic gout therapy.  “Patients who meet one or more of the following criteria qualify for ULT: the presence of tophi, ≥2 acute attacks per year, chronic kidney disease (CKD) stages 2 through 5, and a history of urolithiasis” (Mead, Arabindoo, & Smith, 2014, p 710). If a patient has evidence of tophi, they should continue NSAID therapy for six months after serum urate levels reach target and until tophi resolve or if no tophi, three months after urate levels reach target and no evidence of tophi. 

The first line therapy for chronic gout is Allopurinol taken daily.  Allopurinol is a type of xanthine oxidase inhibitor.  Febuoxstat is in the same category, but is more expensive and the Food and Drug Administration (FDA) warns against hepatic failure while on this medication (Mead, Arabindoo, & Smith, 2014).  Allopurinol should be initiated at 100 mg daily and titrated up by 100 mg every 2-5 weeks until target uric acid levels are reached.  This should be continued indefinitely. In the case of xanthine oxidase inhibitor allergy, Probenecid can be used instead.  Probenecid is an uricosuria agent and should be dosed at 250mg twice a day and titrated until target serum uric acid levels are reached (Mead, Arabindoo, & Smith, 2014).

Patient who fail this therapy should be placed on Pegloticase, which is a new medication that is administered intravenously every two weeks.  This medication is a urate oxidase enzyme that converts uric acid to allatonin, which is then water soluble (Mead, Arabindoo, & Smith, 2014).  This is a VERY expensive medication and should only be used as a last resort to decrease urate levels.  Consider medication noncompliance and re-education before putting a patient on this medication.

Other considerations for managing gout is lifestyle changes with diet.  “A diet extremely high in protein and fat with very little carbohydrate intake may induce ketogenesis, which is known to be an inhibitor of uric acid excretion. Another inhibitor of uric acid excretion is elevated lactate levels, which can be induced by alcohol ingestion. Refined sugar also exacerbates the issue through the increase in dietary fructose” (Connery, 2013, p 24).  Patients with gout should stay away from alcohol, but, if unable to avoid, the safest type is dry wines due to the low alcohol, sugar, and purine content.  Beer is the most unsafe type due to the guanosine (a type of purine) content.  Manufacturers today are adding high fructose corn syrup to everything, but the biggest perpetrator is drinks.  Sugary drinks, including, soda and juice, should be avoided to keep the uric acid levels low (Harvard Health Letter, 2010).  High protein diets that can exacerbate gout attacks include meat and seafood, which should be limited to 0.8g/kg/day (Connery, 2013).

Another factor that should be considered is diuretics.  Hypertension is a significant problem in the adult population and many people are well controlled on diuretics such as hydrochlorothiazide.  But multiple studies have been done that show an increase in gouty attacks while on a diuretic.  A study of almost 25,000 people with gout showed a significantly increased risk of a gout flare-up when a diuretic was used. “Diuretics increase the net reabsorption of uric acid in the proximal tubule of the nephron and thereby reduce urinary excretion and increase the risk of hyperuricaemia and gout.  The increase in serum uric acid concentration and the risk of gout caused by diuretics may be noted within a few days of the start of treatment” (Choi, Soriano, Zhang, & Rodríguez, 2012, p 4).  This study also noted that the use of losartan greatly reduced the amount of serum uric acid by 20-25% by producing a uricosuria effect similar to that of probenecid (Choi, Soriano, Zhang, & Rodríguez, 2012).  Notably, the effect was not found when other angiotensin II antagonists were used (e.g valsartan). 

Role of Nurse Practitioner and Referral

            Nurse Practitioners managing patients with gout should be highly aware and sensitive to an oncoming acute gout attack in their patients.  A good health history during a flare-up is the best way to effectively manage gout.  Patients with chronic kidney disease, obesity, family history of gout, hypertension, and metabolic syndrome should all be considered at high risk for crystalline deposition of uric acid in the joints.  Patients that drink alcohol, especially beer, in addition to these risk factors are at an even greater risk.  Educating patient about their risk will be an essential component of managing this disease.  Diet recommendation is another component.  Low fat, less alcohol, low protein (including seafood), and low fructose should all be considered when educating.  It is important to be specific about what foods to avoid because some people do not understand the crawfish or soda they are consuming is contributing to their gout attacks.  Managing hypertension is another component and this includes ensuring that patients with gout are not taking diuretics that are proven to contribute to this problem.  Using Losartan instead can reduce uric acid levels and keep blood pressure under control.  A referral to an rheumatologist should be made for patients with frequent acute attacks, persons younger than 35, renal insufficiency, and premenopausal women  (Dunphy, Windland-Brown, Porter, Thomas, 2011).  Creating a trusting relationship with patients if the best way to ensure that their gout is managed properly.

Conclusion

            Gout presentation is distinct from other arthritis issues.  It should be managed aggressively and effectively.  Nurse Practitioners are great resources for gout patients because of the preventable nature of the disease.  Education on what foods to avoid and risk factors associated with gout are essential.  Chronic gout is preventable if patients have the right resources and knowledge to manage it.

References

All about gout. (2010). Harvard Health Letter, 35(6), 1-3 3p.

Berdine, H.,  Elisabeth, R., Aukje, M.T.,  Hein, J.,  Eloy, L., Matthijs, J. (2012).  Use of Diuretics and the Risk of Gouty Arthritis: A Systematic Review.  Seminars in Arthritis and Rheumatism.  41(6) 879–889 10p.

Centers for Disease Control and Prevention (2015).  Arthritis Basics: Gout. Retrieved on July 6th, 2016.  http://www.cdc.gov/arthritis/basics/gout.html.

Choi, H. K., Soriano, L. C., Zhang, Y., & Rodríguez, L. A. G. (2012). Antihypertensive drugs and risk of incident gout among patients with hypertension: population based case-control study. BMJ, 344, d8190.

Clark Connery, G. (2013). Renal Nutrition Update. Renal & Urology News, 12(3), 24. 

Dunphy, L.M., Windland-Brown, J.E., Porter, B., Thomas, D. (2011) Primary Care: Art and Science of advanced practice nursing (3rd ed). Philadelphia, PA: F.A. Davis

Hilaire, M., & Wozniak, J. (2010). Gout: overview and newer therapeutic developments. Formulary, 45(3), 84-90 7p.

Mead, T., Arabindoo, K., & Smith, B. (2014). Managing gout: There’s more we can do. Journal Of Family Practice, 63(12), 707-713 7p.

Vannucchi, P. (2012). Understanding, Diagnosing, and Treating Gout. Podiatry Management, 31(4), 191-200 10p.