Lessons for diagnosing, managing acute joint pain
Clinical pearls for frontline PCPs
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A 70-year-old Korean-born man calls in on Monday morning to make an appointment for an evaluation of acute joint pain, which started yesterday. He is in a significant amount of pain and would like to be seen today if possible.
He is booked into one of the physician’s acute slots.
The medical assistant (MA) checks in the patient and notices that he walks with an obvious limp.
- Past medical history reveals hypertension and chronic kidney disease.
- There is no formal diagnosis in the chart of previous gout, pseudogout, joint trauma or fever.
- He currently takes hydrochlorothiazide (HCTZ) 25 mg daily for hypertension and low-dose acetylsalicylic acid 81 mg daily for primary atherosclerotic cardiovascular disease prevention.
The MA performs the gout diagnostic rule test, and the patient scores 13.
The physician reviews the chart and sees that the patient has been seen infrequently over the past 5 years for an occasional acute problem and a physical exam about every other year.
The MA presents the case to the physician: “Doc, this is a 70-year-old male who called in this morning for a 1-day history of severe joint pain. He just got back from a trip to Las Vegas with his college buddies on Sunday AM. They really lived it up there — drank much more beer and spirits than he was used to and ate out every night. He told me that he had not had so much lobster and seafood in years. Anyway, he is miserable. His right big toe is red and swollen, and he has some joint deformities involving some of his finger joints. He has never had joint pain like this. He even said that last night it was “so painful that he could not have a bed sheet touching his big toe because of the pain.”
The physician enters the room and notes that the patient appears to be in moderate distress. He shakes hands with his left hand as his right third proximal interphalangeal joint is swollen and painful. He winces when he stands up and bears weight. She reviews his history, and after a few questions, recalls that he has had perhaps four or five episodes of severe joint pain involving the toes and feet over the past 10 years. He just thought that they were due to “getting old” and did not seem to last for more than a week or two. His physical exam is notable for a red, warm, swollen right first metatarsophalangeal (MTP) joint and a painful, swollen, slightly red, right third proximal interphalangeal joint. Around his elbow and right first MTP, there were spongy nontender lumps that were not red or warm.
Gouty tophi on the elbow of a middle aged male nurse. Image: Nick Gorton/Wikimedia
Perusal of his labs over the past 5 years showed creatinine to be 1.6 2 years ago and 1.8 last year (glomerular filtration rate [GFR] = 37). Blood sugars (BS) on the chem panel have always been less than 100. The basic metabolic panel today showed BS of 78 and creatinine of 1.8 (GFR = 37)
The physician made the presumptive diagnosis of acute exacerbation of recurrent gouty arthritis and started the patient on prednisone 40 mg daily. The patient called in with an update the following day, and he reported about 75% improvement. He called back in 3 days to explain that his pain, redness and swelling had resolved. The physician told his nurse to relay to the patient that he should reduce his prednisone by 5 mg every 3 days until he finishes the prednisone. He was asked to stop his HCTZ. He was advised to make a follow-up appointment in 2 to 3 weeks.
At the follow-up appointment, he was well and free of joint pain. He was given extensive information about gout, including possible dietary triggers. Because of his Korean descent, he was asked to stop at the lab to have a HLA-B*58:01 test done, which came back negative in 4 to 5 days. After the result was known, a prescription for allopurinol 50 mg daily was called in. This was increased to 100 mg daily 1 month later. He was asked to return for a serum uric acid level about 3 months after starting the allopurinol, and the level was 4.8.
Lessons learned
- Gout is very common, especially in men older than 40 years of age and postmenopausal women. Many of these patients have had a long history of elevated uric acid levels without symptoms.
- The diagnosis of gout is made by taking a careful history and physical. The gold standard for diagnosis is to look for negatively birefringent needle-like crystals under a polarized microscope. The gout diagnostic rule can be useful in predicting the likelihood of gout and, in some cases, prevent the need for joint aspiration.
- The differential diagnosis of gout incudes pseudogout (different crystals, different joints, common X-ray findings of chondrocalcinosis), infection (look for open portals of entry, immune compromised state), trauma, and other inflammatory arthritides like rheumatoid arthritis.
- Risk factors for the development of gout include male sex, advanced age, certain medications such as thiazides, loop diuretics, and organ transplantation medications such as cyclosporine A.
- All patients with gout have elevated uric acid, but not all patients with elevated uric acid have gout. Interpretation of serum uric acid during an acute attack can be tricky because it can be normal in a significant number of patients.
- Do not start allopurinol in the “intercritical” period -eg, wait until at least 2 to 3 weeks after the gout flare has passed before starting allopurinol. Aim for a uric acid level less than 6 to reduce the risk for another gout attack (less than 5 for patients with multiple joints affected, documented joint damage, tophi present, recurrent flares or a history of uric acid stones).
- Be alert to the possibility of severe allopurinol cutaneous adverse reactions, especially in those from Korea, Han Chinese patients and patients from Thailand. Consider ordering HLA-B*58:01 gene testing. If positive, do not use allopurinol and consider referral to a rheumatologist for ongoing care.
- Advise the patient to limit or eliminate all alcohol, especially beer and spirits. A low-purine diet is generally no longer recommended unless the patient has recurrent flares. The DASH diet and the Mediterranean diet are better alternatives.
References:
- American College of Rheumatology. Gout. https://rheumatology.org/patients/gout. Accessed Oct. 9, 2023.
- Dalbeth N, et al. Lancet. 2016;doi: 10.1016/S0140-6736(16)00346-9.
- Fenando A, et al. StatPearls. Gout. https://www.ncbi.nlm.nih.gov/books/NBK546606/. Last updated Dec. 27, 2022. Accessed Sept. 29, 2023.
- FitzGerald JD, et al. Arthritis Care Res (Hoboken). 2020;doi:10.1002/acr.24180.
- Jutkowitz E, et al. Semin Arthritis Rheum. 2017;doi:10.1016/j.semarthrit.2016.10.009.
- Pascual E, et al. Nat Rev Rheumatol. 2015;doi:10.1038/nrrheum.2015.125.
- Pittman JR, Bross MH. Am Fam Physician. 1999;59(7):1799-1806.
- Villa-Forte A. Merck Manual. How to do metatarsophalangeal joint arthrocentesis. https://www.merckmanuals.com/professional/musculoskeletal-and-connective-tissue-disorders/how-to-do-arthrocentesis/how-to-do-metatarsophalangeal-joint-arthrocentesis. Reviewed/revised June 2023. Accessed Sept. 29, 2023.
- Villa-Forte A. Merck Manual. How to do metacarpophalangeal and interphalangeal joint arthrocentesis. https://www.merckmanuals.com/professional/musculoskeletal-and-connective-tissue-disorders/how-to-do-arthrocentesis/how-to-do-metacarpophalangeal-and-interphalangeal-joint-arthrocentesis. Reviewed/revised June 2023. Accessed Sept. 29, 2023.
- Williams CJ, Rosenthal AK. Best Pract Res Clin Rheumatol. 2021;doi:10.1016/j.berh.2021.101718.