Gout is a type of inflammatory arthritis that can lead to significant pain and lack of mobility. It occurs when hyperuricemia leads to the formation of crystallized monosodium urate which gets deposited in joints, tendons and bursae, causing swelling and pain. 

Gout can be primary or secondary. The exact cause of primary gout is not fully understood. In most patients, gout occurs due to a decreased excretion of uric acid. In others, it occurs due to overproduction of uric acid. Both pathologies lead to elevated uric acid levels or hyperuricemia. It’s important to note, however, that hyperuricemia on its own does not cause gout. Many people have elevated urate levels and do not develop gout.

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Secondary gout develops as a consequence of another condition. Common conditions that predispose someone to gout include obesity, hypertension, diabetes, heart disease, renal disease, lymphoma, and leukemia. Nutritional factors that can lead to hyperuricemia include excess intake of high-purine foods, fructose and alcohol. This is why the disease was historically called the “disease of kings.” High-purine foods that can trigger gout include organ meats, red meat, shrimp, mussels, lobster, anchovies, sardines, beer, and hard liquor. Moderate-purine foods include oatmeal, spinach, beans and cauliflower, among others.

It can also occur secondary to pharmacological treatment for other conditions. Main culprit drugs are thiazide and loop diuretics, which are often used to treat hypertension and prevent fluid volume overload in patients with heart failure. Other drugs that can lead to hyperuricemia and gout include low-dose aspirin, anti-tubercular drugs, cytotoxic chemotherapy and the immunosuppressants cyclosporine and tacrolimus. 

Certain individuals are at higher risk for the development of gout. This includes males, those of advanced age, postmenopausal women, and individuals from certain ethnicities such as African American, Hmong and Pacific Islanders. 

The four phases of gout

Left untreated, gout progresses through four clinical phases. 

  • Phase 1: Asymptomatic hyperuricemia. In this phase, the patient’s urate levels are elevated, but they have no signs or symptoms of gout.
  • Phase 2: Acute gouty arthritis. In this phase, the patient has swollen and painful joints. It is at this phase that most patients seek medical care.
  • Phase 3: Intercritical gout. This phase can last for months up to years. The patient can be asymptomatic during this phase or have occasional flares. 
  • Phase 4: Chronic tophaceous gout. In this phase (which can occur many years after the first attack of gouty arthritis), clusters of urate crystals called tophi develop in the soft tissues, synovial membranes, cartilage and tendons.

Tophi can damage bone and tissue and even lead to deformity and loss of mobility. Over time the skin over the tophi can degenerate and cause a white exudate to be released.

Complications of gout

In addition to physical disability and pain, gout can also lead to the formation of renal calculi, infections secondary to tophi rupture, atherosclerosis and its sequelae, and nerve damage.

Now that you understand the basics of gout, let’s dive into caring for these patients using the Straight A Nursing LATTE method.

L: How does the patient LOOK?

A patient with gout will be complaining of severe to intense pain in a joint, most often this is first noticed in the metatarsophalangeal joint. The pain usually follows a predictable pattern where it will peak within 24 hours and then gradually resolve over 7 to 10 days. Many patients report the pain starts at night. If you’re reading a chart and you see the term “podagra” this is a medical term meaning the pain is in the big toe, which is a very common site. Other sites are the knees, ankles, elbows and feet.

Depending on the stage of gout, the patient may also have tophi, which can occur in many locations of the body. Common sites for tophi include the pinna of the ear, elbows, hands, knees, feet, lateral forearms, and the Achilles tendon. If a tophi has caused the overlying skin to ulcerate, a white exudate may be present.

A: How do you ASSESS the patient?

Key assessments are centered around the patient’s musculoskeletal status. Look for pain in the 

affected joints as well as ROM to understand how the condition affects the patient’s mobility and ability to perform ADLs. The pain with gout can have a significant impact on quality of life, sleep, social connections and work. It is also beneficial to perform a thorough pain assessment, utilizing a standard format such as the OPQRST format.

O: OnsetWhen did the pain start? Did it come on suddenly or ramp up over time? The patient will often tell you the pain started in the middle of the night and came on suddenly.

P: Provocation and palliationWhat makes the pain worse or better? A patient with gout may state the pain is worse after eating specific foods and that anti-inflammatory medications may help.

Q: QualityWhat is the quality of the pain? Patients with chronic gout may state the pain as a continuous dull aching pain. An acute attack may be described as sharp or even stabbing pain.

R: RadiationDoes the pain radiate anywhere? The pain associated with gout is typically localized to the affected body part.

S: SeverityWhat is the severity of the pain on a 0 to 10 scale?  The patient suffering from an acute attack will report the pain as very severe.

T: TimeHow long ago did the pain start? An acute attack typically resolves within 10 to 14 days, so the answer will vary from patient to patient.

If the patient has ulcerated skin over areas of tophi, examine the exudate for signs of infection. This includes localized erythema, warmth, pain and purulent drainage.

T: What TESTS will be conducted for a patient with gout?

Key tests for a patient with gout include:

  • Serum urate level: Hyperuricemia is present when serum urate is above 6.8  to 7 mg/dL
  • Arthrocentesis: In this procedure, a needle is inserted into the affected joint and synovial fluid or tophi is obtained for examination. Microscopic evaluation can identify the presence of urate crystals and, if present, signs of infection. If the patient has calcium pyrophosphate crystals, the patient has a condition similar to gout, which is called pseudogout.
  • X-ray: X-ray of the affected joints will show damage to bone and cartilage in chronic gout. Tophi are visible as chalky white nodules with a crystalline center.
  • CT Scan: Dual-energy computerized tomography (DECT) looks at the joint from many angles to show the presence of urate crystals.
  • Ultrasound: Ultrasound uses sound waves to detect the presence of tophi or urate crystals in the joints.

T: What TREATMENTS are provided for a patient with gout?

Treatments for gout will depend on whether the condition is acute or chronic. The goals of therapy are to stop an acute attack, reduce urate levels, and prevent future attacks from occurring.

To treat an acute gout attack, both pharmacology and dietary modifications will be utilized. 

  • NSAIDs  – NSAIDs are often used short-term in the treatment of gout for their anti-inflammatory properties. 
  • Corticosteroids – Corticosteroids, such as prednisone, may be used during an acute flare up. Note that corticosteroids come with unpleasant side effects such as weight gain, mood swings, hyperglycemia and hypertension. Longer term use can lead to redistribution of body fat, osteoporosis, poor skin integrity and higher risk for infection.
  • Colchicine – Colchicine disrupts leukocyte activation to disrupt the inflammatory response to monosodium urate crystals. Its use is typically avoided in patients with hepatic or renal impairment and can cause serious hematologic adverse effects including leukopenia, thrombocytopenia, aplastic anemia and agranulocytosis. More common adverse effects are diarrhea, nausea and vomiting. Monitor your patient for colchicine toxicity which includes muscle weakness or pain, tingling in the periphery, bruising or unusual bleeding, signs of significant anemia, and severe vomiting or diarrhea.
  • Dietary modifications – The patient should follow a low-purine diet and abstain from other triggering items such as fructose and alcohol.
  • Non-pharmacologic therapies – These include cold therapy, elevation and immobilization in some cases.

Other medications are utilized to block uric acid production or improve the removal of uric acid by the kidneys. 

  • Allopurinol and febuxostat block uric acid production. Allopurinol is a xanthine oxidase inhibitor and the most commonly used medication to treat chronic gout. It is also used to treat hyperuricemia secondary to the treatment of leukemias and tumors. Common adverse effects of this medication include rash which could be a sign of a potential serious reaction such as Stevens-Johnson syndrome. If a patient develops a rash while taking allopurinol, the medication will likely be discontinued. The patient should increase their hydration to help prevent the formation of calculi, especially when combined with a uricosuric medication such as probenecid. Click here to learn more about allopurinol.
  • Probenecid is often used to treat hyperuricemia secondary to thiazide therapy and is a uricosuric medication, meaning it promotes renal excretion of uric acid. Patients should maintain adequate hydration to prevent the formation of uric acid stones.
  • The IV medication pegloticase may be used for gout that is refractory to treatment or in those who cannot take xanthine oxidase inhibitors such as allopurinol. Serious reactions can occur including anaphylaxis, hemolysis and methemoglobinemia.

Lifestyle modifications for gout

A key component of gout therapy is dietary modification. Patients will be counseled to avoid high-purine foods and to have moderate-purine foods only occasionally. They should also avoid high fructose beverages and alcohol, especially beer and hard liquor. 

Lifestyle modifications are aimed at reducing weight and improving mobility with exercise. Good options for a patient for gout include low-impact activities such as swimming, cycling and walking. 

E: How do you EDUCATE the patient?

Since gout can be a chronic condition that requires careful management, education will play a key role in preventing further progression of the disease and gout flares. 

  • Teach the patient to keep a food journal. Not only can this help them adhere to dietary guidelines, it can also help them identify their specific trigger foods.
  • Teach the patient that dehydration can worsen gout. Staying hydrated promotes uric acid excretion and helps prevent complications due to the formation of renal calculi.
  • Teach the patient that allopurinol will not stop an acute attack, but is used long-term to prevent future attacks from occurring.
  • Teach the patient that sometimes allopurinol can trigger an acute attack when starting therapy. This is due to crystals lodging in joints as they are made smaller. The patient may receive another medication such as an anti-inflammatory to help reduce the risk of an acute attack occurring.
  • Teach the patient to notify their medical provider of any other medications they are taking. Some may increase the risk for hyperuricemia and increase flares of gout. 
  • And, ensure the patient understands the importance of and how to follow their treatment plan. According to a 2020 study, less than 50% actually follow their urate lowering therapy plan long term

Take this topic on the go by tuning in to episode 296 of the Straight A Nursing podcast. Listen from any podcast platform, or straight from the website here.

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