Today’s morning report involved an 87-year-old woman with a history of gout, hypertension, dyslipidemia and chronic kidney disease who was admitted with a polyarthritis impairing her ability to ambulate. It involved one knee, and several small joints in the hands and wrists.
We talked about a number of valuable learning points related to monoarthritis, although technically this would have been a polyarthritis.
-Monoarthritis is a very common reason for emergency department presentation and can be divided into its usual causes.
· Infectious – which can be divided into gonococcal and non-gonococcal infectious arthritis. This is essentially an emergency because delays in therapy can be “joint threatening” and early diagnosis and management (which may include orthopedic consultation and washout/surgery) is essential.
· Crystalline – This may include gout or calcium pyrophosphate (pseudogout). The biggest clue that this may be going on is probably that the patient has a history of having had gout before. Though classically thought of as a monoarthritis, polyarticular flares of crystalline arthritis are not uncommon.
· Hemarthrosis – this may occur spontaneously if patients have bleeding diatheses or are on anticoagulation or with minimal trauma. Treatment is typically supportive.
· Internal derangement of the joints – this can occur with minor trauma or meniscal injuries in structures like the knee.
· Inflammatory arthritis – this is a less likely cause of a monoarthritis, as most of the inflammatory seropositive conditions would cause symmetrical small joint inflammation, but certain conditions can give monoarthritis presentations.
· Trauma/Osteoarthritis – Though OA is thought of as a degenerative type of arthritis, there can be “acute flares” of OA which lead to joint effusions and pain with ambulation.
-We spoke about acute and chronic management of gout flares. Generally speaking, the paradigm is that measurement of the uric acid level during an acute flare is not helpful. That said, rheumatologists seem to order them every time gout is suspected. The reason we are all taught not to do this, is that gout flares can lead to shifts in the level of serum urate, making the test an unreliable predictor of how much uric acid is actually in the joint.
-The management of acute gout centres around anti-inflammatory therapy. If patients can tolerate NSAIDS, which very few of our patients can, then two weeks of indomethacin or naproxen can make all the difference. Many patients cannot tolerate NSAIDS and may be better off with steroids. Typically, for monoarticular gout in an injectable joint, injections of methylprednisolone are very effective and minimize the systemic side effects of steroids. In the case of polyarticular gout, oral steroids may be a better option. Colchicine is a microtubule stabilizer that may be helpful in the acute therapy of gout, but trial data are limited. Anecdotally, rheumatologists seem to use this drug in the early therapy of gout (i.e. within 24 hours of symptoms) until discharge from hospital. The drug has numerous side effects the most notorious of which is diarrhea. It cannot be used in those with renal or hepatic failure.
-Never start treatment with uric acid lower therapies when patients are having a gout flare. Likewise, it is probably not a good idea to stop uric acid lowering therapies in that setting either. These can lead to shifts in the amount of uric acid and precipitate crystallization in joints (i.e. a gout flare).
-Uric acid lowering therapy, for many years, was accomplished with Allopurinol. There are a number of “habits” that one should use when prescribing allopurinol (or uric acid lowering therapy) for anyone (Credit to Dr. S. Carette for teaching me this)
· Allopurinol is lifelong therapy, so it must only be used in patients with recurrent gout (many would say more than 3 or 4 attacks that are disabling)
· Allopurinol must always be dosed in accordance with renal function
· Dosing must be titrated to the uric acid level (target under 350) and there is generally no uric acid level that is “refractory” to an adequate amount of allopurinol
· Uric acid lowering therapy is indicated for those patients with tophaceous uric acid deposits, joint destruction as a result of gout, renal insufficiency, uric acid nephrolithiasis, and very high amounts of urate excretion in the urine
· Febuxostat is a new uric acid lowering agent that is not more effective, despite being vastly more expensive, than allopurinol. Allopurinol has numerous side effects but the most significant are DRESS or skin reactions like SJS. In those circumstances, and in patients who can afford it, febuxostat may be a reasonable option.
· Don’t forget that, for whatever reason, losartan has some urate lowering effect so patients with indications for it (e.g. hypertension) may actually benefit from this agent over other ACE inhibitors or ARBs
-In patients with a life-threatening urate level, such as those with tumour lysis syndrome, we use agents that actually catalyse hydrolysis of uric acid rather than prevent its formation. Humans, for some reason, are one of the only mammals without an endogenous enzyme to do this. The product formulation that we use is Rasburicase from Aspergillus flavus. A new agent called Pegloticase is now available, with pig uricase, for those with refractory gout despite maximal urate lowering therapy.
-We spoke briefly about examination of the knee. Specifically, we discussed physical examination menoeuvers to detect a joint effusion.
· The “Bulge Sign” or “Milking” sign involves milking fluid upward and away from the medial portion of the knee, and then tapping or sweeping the lateral aspect of the knee and watching for a small bulge in the medial aspect indicating fluid
· The “balloon sign” involves pressing with one hand against the suprapetallar bursa to compress fluid in the the knee compartment, and placing the other hand just below the patella to feel fluid pushing against it when it is pushed down by the first hand. This detects only relatively large effusions.
· The “ballottement” or “patellar tap” sign involves compressing the fluid from both the cranial and caudal portions of the knee under the patella and then pushing firmly on the patella until you feel it “knock” or “tap” against underlying bone. In a normal knee, there is very little downward excursion of the patella when you do this.
-These terms and names are from Bates guide to physical examination.
Bickley, L., & Szilagyi, P. G. (2012). Bates' guide to physical examination and history-taking. Lippincott Williams & Wilkins.
Becker, M. A., Schumacher Jr, H. R., Wortmann, R. L., MacDonald, P. A., Eustace, D., Palo, W. A., ... & Joseph-Ridge, N. (2005). Febuxostat compared with allopurinol in patients with hyperuricemia and gout. New England Journal of Medicine, 353(23), 2450-2461.
Ma, L., Cranney, A., & Holroyd-Leduc, J. M. (2009). Acute monoarthritis: What is the cause of my patient's painful swollen joint?. Canadian Medical Association Journal, 180(1), 59-65.
Schlesinger, N., Yasothan, U., & Kirkpatrick, P. (2011). Pegloticase. Nature Reviews Drug Discovery, 10(1), 17-18.