Neal Birnbaum, MD
Dr. Birnbaum began with the differential diagnosis of acute monoarthritis, which is one of the more common reasons for inpatient rheumatology consultation and includes crystalline (e.g., gout), septic, autoimmune (psoriasis), traumatic, and hemorrhagic.
The synovial fluid will give an idea as to whether one is more likely than the other, he said. Normal synovial fluid is transparent, clear, has a low cell count, and is very viscous in nature. Noninflammatory etiologies (osteoarthritis) will have some cells but will largely be similar to normal synovial fluid. Inflammatory causes will have higher cell counts (2-10K WBC) but will have much lower viscosity. Septic joints will look pustular with very high cell counts (sometimes too high to be recorded) and will be positive on fluid culture (unless the patient has already received antimicrobial therapy). Hemorrhagic fluid will look like blood, and the history will give clues as to whether that is the case (recent trauma, history of hemophilia).
Gout can manifest in the typical area of the first toe (podagra), Dr. Birnbaum said, but can also appear in less common areas like the distal interphalangeal joints. One may see this more frequently in postmenopausal women, those on diuretics, and patients with renal insufficiency. The diagnosis can be made using a polarizing microscope showing positively bifringent, needle shaped crystals. It is important to be sure that the provider or the lab is able to process the specimen quickly because crystals in synovial fluid tend to dissolve within a few hours after being drawn.
Pseudogout (CPPD) is more likely to manifest in different joints (knees more so than wrist more so than shoulders/hips). One should suspect pseudogout in patients with acute arthritis in patients more than 70 years old. Crystals will be positively bifringent and more rectangular or square shaped, compared with gout crystals. Finding chondrocalcinosis on x-ray on a symptomatic patient can make the diagnosis much more likely. However, a patient can have chondrocalcinosis on an x-ray and not have CPPD. A patient can also have no chondrocalcinosis and have CPPD. It is the combination of the x-ray sign and symptoms that creates the high accuracy of the test.
The treatment for both in the acute setting includes colchicine (2 tabs x 1, then 1 more 1 hour later), NSAIDS (although may not be ideal inpatient because of potential toxicities), and corticosteroids (this can be either oral [prednisone 40 mg q24 with rapid taper], intraarticular [triamcinolone 10 mg-40 mg depending on the joint size], or IV [solumedrol or solucortef equivalent to prednisone 40 q24]).
For management of gout chronically, one should strive for a uric acid level of less than 6.0. Contrary to what is commonly believed, one can start urate lowering agents like allopurinol acutely (start with 100 mg for 2 weeks, then titrate up every 2 weeks until one hits the target uric acid level). Clinicians can consider using febuxostat for those patients who have renal insufficiency. While on the urate lowering agent, use low dose colchicine or NSAIDS for the first few months. Unfortunately, there is no long-term chronic strategy to prevent pseudogout flares. If there is an underlying cause for the pseudogout, then try to address it.
Consults for positive antinuclear antibodies (ANA) are common reasons for rheumatology referrals. The patterns of the ANA and the titer are important to the differential diagnosis. Up to 30% of healthy individuals have a positive ANA. ANA can be helpful as a rule out test for systemic lupus erythematosus (SLE), as it has a high sensitivity and a low specificity. However, because SLE is a clinical diagnosis and because of the high ANA positivity in the population, a high ANA alone does not prove a patient has SLE.
Concerning vasculitis, Dr. Birnbaum recommended thinking about it in terms of small versus large vessel disease. For initial evaluation, one should draw a CBC, erythrocyte sedimentation rate/C-reactive protein, urinalysis, chemistry panel, ANA, antineutrophil cytoplasmic antibodies, rheumatoid factor, hepatitis C antibody, and complement levels (C3, C4, CH50). One can also think of drawing cryoglobulins, especially in settings where one is suspicious that hepatitis C may be present. The differential diagnosis for vasculitis includes drug reactions, infections (mostly viral), malignancy, collagen vascular disease, and idiopathic causes (33%-50% of cases). The treatment is to remove offending agents (i.e., drug-induced vasculitis), treat infections (if applicable), and use steroids (the dosing depends on the situation).
Dr. Birnbaum finished with two relatively new illnesses that should be on clinicians’ radars. Chikungunya virus is transmitted by mosquitoes in the same distribution that one may see Zika virus. The symptoms include headaches, fevers, extreme joint pain, and joint swelling (this aspect is different from many other viral illnesses). The illness is usually acute. However, some patients will continue to have symptoms for up to a year. There is no specific treatment other than symptom relief (pain medications, NSAIDs).
Finally, immunoglobulin G4–related disease can affect virtually any organ system, but seems to manifest frequently as pancreatitis in the hospital setting. Think about this in patients with pancreatitis not secondary to the usual alcoholic or gallstone variety. The gold standard for diagnosis is biopsy with histologic findings of IgG4 in plasma cells. Most patients will be noted to have elevated IgG4 levels. The treatment is prednisone 40mg q24 with a taper over 2 months. For those who cannot be weaned or for those with recurrent disease, rituximab (1000mg IV x 1 then approximately 2 weeks later) can be used.