Gout: Clinical sciences

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Gout: Clinical sciences

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Attention deficit hyperactivity disorder (ADHD): Clinical sciences
Premenstrual syndrome (PMS) and premenstrual dysphoric disorder (PMDD): Clinical sciences
Alcohol use disorder: Clinical sciences
Alcohol withdrawal: Clinical sciences
Selective serotonin reuptake inhibitors
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Serotonin and norepinephrine reuptake inhibitors
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Osteoporosis: Clinical sciences
Mechanical back pain: Clinical sciences
Gout: Clinical sciences
Calcium pyrophosphate deposition disease (pseudogout): Clinical sciences
Osteoarthritis: Clinical sciences
Inflammatory myopathies: Clinical sciences
Osteomyelitis: Clinical sciences
Septic arthritis: Clinical sciences
Compartment syndrome: Clinical sciences
Anatomy clinical correlates: Bones, joints and muscles of the back
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Antigout medications
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PDE5 inhibitors
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Coxiella burnetii (Q fever)
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Antihistamines for allergies
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Benign skin lesions: Clinical sciences
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Decision-Making Tree

Transcript

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Gout is an acute inflammatory arthritis that occurs when monosodium urate crystals deposit in joints, soft tissue, and bones. This is typically associated with hyperuricemia due to either underexcretion or overproduction of uric acid.

Risk factors include male sex, obesity, drinking too much alcohol, consuming certain foods like red meat and seafood, as well as dehydration, taking diuretics like thiazides, and increased cell turnover like in hemolysis or tumor lysis syndrome.

The diagnosis of gout is made clinically and relies on the presence of classic symptoms, known risk factors, and lab findings. However, in some cases when the diagnosis is not clear, joint aspiration may be needed.

Alright, if a patient presents with signs and symptoms suggestive of gout, you should first perform a focused history and physical examination. As well order labs like a serum urate, CBC, ESR, and CRP.

Your patient may report rapid onset of redness, pain, and swelling in a joint, most commonly involving the big toe, but can involve other joints, such as the knee.

This is especially common after drinking alcohol, or consuming purine-rich foods like red meat or seafood. Other risk factors include high fructose intake, diuretic use, obesity, history of diabetes, hypertension, and chronic kidney disease.

Physical exam usually reveals redness, tenderness, and swelling in the involved joints, most often in the first metatarsophalangeal joint. You may also see subcutaneous nodules, or tophi, on the joints and pads of the digits.

As far as labs go, the serum urate will often be elevated, greater than 6.8 milligrams per deciliter, but keep in mind that urate levels can be difficult to interpret during a gout flare.

CBC typically reveals an elevated leukocyte count and inflammatory markers, such as ESR and CRP. If you see this constellation of signs, symptoms, and lab findings, you can diagnose acute gout.

Now lets look at patient with a different but similar focused history and physical results. If your patient reports joint redness, pain, or swelling; but has no obvious risk factors for gout; physical exam reveals redness, tenderness, or swelling, but no tophi present; and if the serum urate, and inflammatory markers are normal Then you should suspect arthritis. In this case, additional tests are needed to diagnose the type of arthritis.

Specifically, perform a joint aspiration of the synovial fluid. If the synovial fluid contains no negatively birefringent needle-shaped crystals, consider an alternative diagnosis, like pseudogout, septic arthritis, or Lyme arthropathy.

However, if the microscopic synovial fluid shows negatively birefringent needle-shaped crystals with possible yellow cloudy fluid that contains white blood cells, you can diagnose acute gout.

Here’s a high yield fact! Pseudogout is characterized by calcium pyrophosphate crystals, which are rhomboid shaped and positively birefringent crystals, and can help differentiate gout from pseudogout.

Alright, now that you’ve diagnosed acute gout, let’s turn our attention to management. Within the first 24 hours of symptoms, begin pharmacological management and start your patient on anti-inflammatory medications for at least 7 to 10 days.

Commonly used medications include NSAIDs, like indomethacin or naproxen, but colchicine can also be prescribed.

If your patient has impaired renal function or cannot tolerate NSAIDS or colchicine, give an oral or intra-articular glucocorticoid instead.

Keep in mind that you should avoid glucocorticoids if you suspect a concurrent infection or if your patient has brittle diabetes.

You should also review your patient’s medication list, and if they are taking a diuretic, discontinue it or adjust the dose.

Next, counsel your patient on non-pharmacologic treatment options, like resting the affected joint and applying topical ice packs.

Sources

  1. "2020 American College of Rheumatology Guideline for the Management of Gout [published correction appears in Arthritis Care Res (Hoboken)" Arthritis Care Res (Hoboken) (2020)
  2. "Diagnosis and Management of Gout: Clinical Practice Guidelines" Ann Intern Med (2017)
  3. "Gout: diagnosis and management-summary of NICE guidance" BMJ (2022)
  4. "2015 Gout classification criteria: an American College of Rheumatology/European League Against Rheumatism collaborative initiative" Ann Rheum Dis (2016)
  5. "Harrison's: Principles of Internal Medicine" McGraw-Hill Education (2018)