The Physician Assistant Exam will have plenty of questions about pain, including monoarticular arthritis. Talk about pain, and nine times out of ten someone will tell you that three of the most painful things in medicine are childbirth (well, men are just guessing about this), a kidney stone, and an acute gout flare. There are two common causes of acute monoarticular arthritis: gout and pseudogout.
Get a grip on gout on the PANCE
Gout is caused by the deposition of uric acid crystals into a joint space. The most common place is the first metatarsophalangeal (MTP) joint — you can call it the hallux, the big toe, or the great toe. Whatever you call it, gout can hurt like hell. In some stories, gout is so painful that even putting a bedsheet over the affected foot causes the person to scream in pain.
Depending on the severity of the gout, it can also present in the knee or other joints. Understand that gout is more than just uric acid crystals in the joint — it’s a deforming arthritis.
Gout is more common in men. It’s thought that either the body produces too much uric acid or the kidney isn’t excreting enough uric acid. Risk factors for the developing gout include alcohol use, increased purine intake (such as from meat), and diuretics that can deplete volume. Any of these factors can cause a gout exacerbation. Recall that one of the side effects of the diuretic hydrochlorothiazide (HCTZ) is hyperuricemia.
On physical examination, if a joint has significant uric acid deposition, you can see tophi around the joint.
The diagnosis of gout (or pseudogout) is obtained by tapping the joint. As with pleural effusion, the nature of the synovial fluid tells you what you’re dealing with. Tapping the joint is simple, and it provides a big payoff for the PANCE. With gout, you see needle-shaped negatively birefringent crystals. The synovial fluid may show an elevation in the white blood cell count as well.
The serum uric acid level is notoriously unreliable during an acute episode of gout — it can be high, low, or normal. The goal of treatment over time, however, is to reduce the uric acid level to less than 6.5 mg/dL and keep it there. This level minimizes the risk of future attacks.
During an acute flare of gout, treatment options include colchicine, indomethacin (Indocin), and/or steroids. Steroids can be given orally for a steroid taper or injected directly into the joint during an acute flare. Be careful using NSAIDs if the patient has underlying kidney disease.
The treatment for chronic gout is adhering to a low-purine diet and avoiding alcohol. Medications such as allopurinol (Zyloprim) and febuxostat (Uloric) work by inhibiting the formation of xanthine oxidase, an enzyme that breaks down purines.
During an acute gout attack, never give allopurinol as initial therapy. You’ll only make a gout flare worse. However, if a person’s already on allopurinol, don’t stop it. Allopurinol doesn’t relieve acute attacks of gout, but you can use it to treat chronic gout.
How to detect pseudogout
Pseudogout is also known as calcium pyrophosphate deposition disease (CPPD). Whereas with gout you have uric acid deposition, pseudogout involves the deposition of crystals of calcium pyrophosphate dihydrate. The initial presentation can be very similar to gout, with incredible pain and swelling in a joint.
With pseudogout, synovial fluid examination reveals positively birefringent crystals that are shaped like rhomboids. In contrast, with gout, you see negatively birefringent crystals under polarized light.
Pseudogout has a classic radiologic appearance: Because of calcium deposition into the joint, you see chondrocalcinosis. In English, this means that in a radiograph of someone diagnosed with pseudogout, you’d see what looks like a thick chalk line drawn along the affected joint.
The treatment for pseudogout is supportive, similar to the treatment of acute gout. Treating acute pseudogout can include NSAIDs like indomethacin (Indocin) and/or steroids (either oral or via intra-articular injection). Look for an associated condition, especially hemochromatosis or primary hyperparathyroidism.
You’re evaluating a 40-year-old man who presents with a hot, swollen left knee. He doesn’t have a history of gout. On exam, the knee is tender and warm to the touch. Flexion and extension is limited due to pain and swelling. The joint is tapped, and the white cell count is 100,000/μL with more than 80 percent polymorphonuclear leukocytes. There are no crystals seen on the synovial fluid analysis.
What is the likely cause of the knee pain and swelling?
(A) Gout
(B) Pseudogout
(C) Rheumatoid arthritis
(D) Septic arthritis
(E) Reiter’s syndrome
The answer is Choice (D), septic arthritis. Septic arthritis involves a significantly elevated white blood cell count with a neutrophilic predominance in the joint. It can present clinically the same as gout and pseudogout; the key is in the synovial fluid analysis. A common cause of monoarticular joint sepsis is gonococcal infection, particularly in a younger adult. Other common causes of a septic joint are Staphylococcus aureus and Streptococcus species.
Because you see no crystals in the synovial fluid, this man has neither gout nor pseudogout. Rheumatoid arthritis can present with monoarticular arthritis, but it’s rare, and you should see other features of this condition for Choice (C) to be right. The synovial fluid count would not show a left shift or bandemia in rheumatoid arthritis.
Reiter’s syndrome, Choice (E), is a reactive arthritis and usually demonstrates the quatrad of arthritis, conjunctivitis, urethritis, and dermatitis. Lyme disease can also present as an acute monarticular arthritis.
