Clinical quiz 1: Granny’s knobbly fingers *updated*

Just a quick one, but I’m trying to include a bit more clinical content on my blog. Let’s see how it goes!

IMG_0387

An 84 year old woman has an 8 week history of gradually worsening tender lumps on her fingers, R>L. She has not had anything like this previously. She has a history of AF, angina, OA and previous AAA repair. Her medications include warfarin, amiloride hydrochlorothiazide, celecoxib, paracetamol, felodipine, GTN spray, tramadol, allopurinol and she is wearing a buprenorphine patch.

Questions:

1. What is the most likely cause?

2. What are some differential diagnoses?

3. What is the management?

Answer in the comments below, discussion to follow next week!

Granny enjoying a visit from her twins grandkiddies.

Granny enjoying a visit from her twin grandkiddies.

Thanks to my lovely Granny for letting me photograph her fingers! 

**UPDATE: Discussion

Thanks to everyone who commented below and sorry about the delay in updating the post with discussion. I’ve been having some technical difficulties in establishing a reliable internet connection in my new posting in Albany. Particular thanks to my old med school chum Dr Andy Lim who is an advanced trainee in rheumatology and provided a great and comprehensive answer below and also directed me to some useful resources.

Here’s my summary of the learning points:

1 & 2. All of the commenters mentioned the likely suspects with regard to subcutaneous nodules including:

  • Heberden’s nodes of OA – but less likely to occur over such a short time frame and be tender
  • Rheumatoid nodules – which are more likely to occur on the PIP and MCP joints rather than the DIPs in the hands
  • Psoriatic arthritis – but there is no history of rash in this case
  • Pseudogout – but more likely in larger joints
  • Gouty tophi – I think the general consensus is that this is the most likely culprit here!

UpToDate tells me that there are two main subgroups of patients who develop tophaceous gout. One group is represented by men with risk factors of excess alcohol consumption, diuretic use and poor compliance to medication. The second group is (mainly compliant) elderly women with the triad of underlying osteoarthritic finger joints, diuretic use and impaired renal function. We can probably assume that Granny Wilson ticks most, if not all of those boxes!

3. I refer you to Minh Le Cong’s recent foam4gp presentation which summarizes nicely the management principles of acute and chronic gout management and links to further reading.  http://foam4gp.com/2013/03/24/gout-in-6-minutes-for-the-gp/#more-101

I think that this case highlights a few particular management issues which I’ll just briefly mention:

  • Oldies are not always the best historians and may well be on multiple medications that they don’t know the reason for. This is a common challenge when dealing with patients who may be away from their usual clinic and it sometimes requires some lateral thinking to get to the bottom of the relevant clinical background. A quick phone call to the usual treating doctor may be in order if something doesn’t add up.
  • Treat gouty tophi as per chronic gout with uric acid lowering agents. Start allopurinol at 100mg/day and increase 50-100mg monthly, while keeping a close eye on uric acid and LFT/UEC. Aim to get the uric acid <0.36. Cover with colchicine low dose until target is acheived.
  • Treat painful inflamed gouty tophi as per acute gout, eg with NSAID or if contraindications (eg angina as with this case) colchicine in the low dose regimen, ie 2x 500mcg colchicine stat, followed by a further 1x500mcg 1 hour later, and do not repeat for at least 3 days. The old days of bombarding the patient with colchicine every few hours until they got the runs are over. Short course of prednisolone may also be useful.
  • Stop any precipitating medications – in this case, the diuretic is probably doing more harm than good.
  • Look to lifestyle factors. As it happens, Granny is very partial to a big feed of seafood and just the day before the photos were taken we had dined on crabs, prawns and crayfish. I may have to have a word with her about cutting down on the crustaceans which I don’t think will impress her very much!

Some further reading:

  1. EULAR Evidence Based Guidelines for Gout: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1798308/
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4 thoughts on “Clinical quiz 1: Granny’s knobbly fingers *updated*

  1. Poor old granny’s fingers look sore! My main suspect would be Heberden’s nodes of Osteoarthritis and an acute flare. However, a subacute history doesn’t fit perfectly with this. I’d also consider gouty tophi and pseudogout as differentials…
    Treatment options are tricky because Granny already on quite a lot of Rx:-
    1. Regular paracetmol should be continued
    2. NSAID – given AF, angina and previous AAA I’d be nixing the celecoxib, and switching to ibuprofen or naproxen +/- PPI if necessary. Whether NSAIDs should even be a long term therapy is a quality of life versus CV risk discussion that needs more detail and another day 😉
    3. If thinking gout, stop the allopurinol
    4. Consider a short term increase in opioids if pain bad
    5. Interphalangeal joint injection is an option, but beyond my skill, particularly in those swollen DIPJs!
    6. I know my local rheumatologist (Kempsey has two physicians only, Rheum and Cardio, go figure!) might trial prednisone instead, not sure of the evidence of this though

    PS Is Granny right hand dominant?

  2. Granny has a subacute polyarthropathy involving primarily the DIP and less so the PIP joints. It does have a bilateral nature though prominent on the R. The tender nature indicates an inflammatory component. She has never had this before. I would be curious whether she has any other joint inflammation eg. shoulders, hips and back. Also whether she has any psoriasis patches. Further, if she had recently had a viral illness (eg. reactive).

    She does have a wide differential.
    Osteoarthritis – appears like heberden’s nodes however given their subacute presentation this makes this far less likely. Also the amount of deformity is significant and I am sure she may have noticed this in the preceeding years. Also, not usually a significant inflammatory component acutely to these.

    Rheumatoid – Very late presentation and not the typical locations eg. MCPs. and once again the deformities appear quite significant for only an 8 week presentation

    Gout/Pseudogout – probably the most likely presentation. Given that she is on allopurinol I would be curious as to why she is on preventative medication for gout if this has not happened before eg. usually requires multiple episodes of gout for a doctor to start allopurinol (unless on it for another unmentioned reason). From the pictures it does look possibly like she may have some white urates under the skin but this would be easier to see on examination. If this is chronic gout with an acute flare in spite of allopurinol I would be curious to see what her renal function is given she is on some medications which will decrease her GFR and decrease her renal excretion of urates. Thiazides can worsen gout, she is on NSAIDs and she is a vasculopath (AAA) and she is 84, all of which may contribute to worsening renal function. Also the underlying history of mild OA means these joints are more prone to gout.

    Other things could be reactive arthritis (reiters formerly) (not usually this location and more inflamed and less degenerative) or psoriatic (not the classic dactylitis).

    Management (assuming gout worsening secondary to renal impairment – which could be checked with urate level and ELFTs) would be to maximise her renal function through changing celecoxib to paracetamol osteo, consider ceasing the thiazide (which can worsen gout) or changing to an ACE (depending on K+ history, to protect the kidneys) and then considering ceasing the amiloride also (if renal function has gone off her K+ could be high). She needs rationalisation of her analgesia also because the tramadol is not a good PRN with a buprenorphine patch (and I don’t like it in the elderly) but the buprenorphine is a good choice if renal function is not strong. Up titrating her patch to help control pain would help. Depending on her BP you can consider pred course, and then referral to a rheumatologist for consideration of further treatment of her ?gout +/- joint injections. Only other thought is why is she not on a beta blocker given AMI history? Perhaps she has a history of slow AF?

  3. Hi Penny,
    Sandra has put me up to the challenge so I will attempt to answer your questions!

    You may have to ask your grandma a few questions to help me out- are her symptoms inflammatory (morning stiffness duration etc), and are you certain the history is of 8 weeks duration only, or do you think maybe longer? Also, as Rob says, it would be of interest to find out why she is on allopurinol- presumably for previous symptomatic hyperuricaemia (renal stones or previous gout in other joints)?

    As for your questions;

    1. What is the most likely cause?
    – The DIP involvement makes RA pretty unlikely. OA nodes (ie. Heberdens) tend to be quite hard and surprisingly, not that tender. Tenderness indicates probable synovitis and therefore you would think this is inflammatory. Although there is a subset of inflammatory OA is more common pre/perimenopausal. Crystal deposition disease (i.e. gout/pseudogout) would be high on my list of differentials. I would favour gout as pseudogout tends to cause a larger joint arthropathy (shoulders/knees) but when it does occur in hands, ususally the 2nd/3rd MCPs are affected. The appearance of the nodules (whitening- I think I can see it) are most typical of gouty tophi.
    Psoriatic arthritis can affect DIP joints, but without a history of psoriasis and for the reasons above, this does not appear to be psoriatic arthritis.

    2. What are some differential diagnoses?
    – See above

    3. What is the management?
    – Assuming this is gout, and quite active, I would check your grandma’s bloods incl LFT, UEC, CRP, ESR, and serum urate. (Maintain her allopurinol- dont stop it).

    Assuming no contraindications (ie. renal dysfunction), I would start colchicine 500mcg BD or TDS (for acute gout). Monitor for GI upset (D&V and dose reduce).
    Given her history of angina, I would avoid NSAIDs (including celecoxib).

    When most of her acute synovitis has settled, I would then reduce her colchicine to 500mcg daily and increase her allopurinol (assuming no renal or hepatic dysfunction). The target serum urate is <0.36, so titration of her allopurinol should occur monthly by 50-100mg (again depending on her renal function).

    Tophi tend to take 18 months or longer to resolve (assuming a good dose of allopurinol). The commonest issue I see of patients referred to me with ongoing gout despite allopurinol, is too small a dose of it. Allopurinol hypersensitivity syndrome is not as common as people think (again, with careful monitoring of LFT/UEC).

    After she has reached a stable serum urate, you can stop the once daily colchicine.
    (ie. she may be on colchicine for 3 months).

    Xrays of her hands and feet may be helpful if they show juxta articular erosions.

    Also, look at her diet – red meat, crustaceans, beer (more than wine/spirits). If she doesnt need the diuretics, then reduce/cease them. Losartan is the only antihypertensive with favourable outcomes in reducing serum urate.

    Hope that helps.

    Andy

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