I have noticed something that I have never seen talked about in Hand Surgery Society meetings. And I don’t quite know how to research it.
Something that is very well recognised is that DeQuervain’s is very common in people who pick up small children. It used to be almost exclusively mothers of small children. Most often the first child, but not always. More recently, I have seen it in ‘hands-on’ fathers, grandparents and nursery workers (as small children are increasingly looked after by people other than their mothers!). I have also seen it in the proud owner of multiple puppies. And people who pick up large items like Lever Arch files.
The condition often settles spontaneously, but can become a persistent nuisance. It rarely endures for longer than about two years. If untreated, it probably will settle over a year or two, or until the causative activity ceases.
You might expect, then, that I might see the condition recurring in a patient who has a second child, or subsequent children. The odd thing is that I cannot remember seeing a patient presenting to me in that way.
I see this condition almost every week. So that’s probably about 40 a year. I do steroid injections on most. A second steroid injection is required about 20% of the time because of recurrence (usually when the steroids wear off at around two months post injection). About half of those go on to not need any further help. That leaves about 4 a year who resort to surgical decompression (after second recurrence of symptoms).
So, in the last 20 years, you might think many of the (probably around 800) patients I will have seen with this condition, might have (a) had a second/subsequent child, and (b) developed a recurrence.
Why might this be?
- Patients so disliked the experience of being treated by me they would never come back?
- The condition didn’t come back?
So why might it not recur?
When we do a surgical release, it is clear that the ‘retinaculum’ (the membrane over the tendon at the wrist that hold the tendon close to the bone and prevents ‘bowstringing’ under the skin) is very thick. It is normally less than a millimetre thick in the absence of this condition, but becomes very hard and about 2mm thick when it has been inflamed for some time.
The condition is a very basic mechanical principle of a tunnel being too tight for the tendon to pass through it without touching the sides. Imagine a train rubbing the sides of a tunnel causing trauma to the train and the tunnel walls.
My hypothesis then, and this is difficult to prove, is that when the tendon swelling goes down, either naturally or with steroid injection, but the retinaculum tunnel stays larger than it needs to be (having been stretched by the swollen tendon) and is stiff. It is therefore expanded to a larger capacity than the tendon passing through it needs (by just a small amount) and therefore much less likely to constrict the tendon again.
Recurrence after successful surgery is also something I haven’t seen (though I have seen incomplete recovery after surgery). That is presumably for the same reason, as the surgery is designed to open the retinaculum and let it heal so that the space in the tunnel is larger than it was.
We have, in surgery, used ‘tissue expanders’ to create larger spaces for later surgery. These are inflatable devices. I suspect that the swollen tendon acts as a tissue expander within the tunnel, and when the swelling goes down, it therefore has ample room in the future and doesn’t ever become too swollen to slide through the tunnel again.
This is difficult to prove. A survey of patients would be unlikely to detect people who had not had recurrence with subsequent children. The sample sizes would need to be very big, and response rates would likely be low (the research question doesn’t seem important enough).
MRI scans are also too low resolution to allow measurement of cross sectional area on a tunnel which is only about 0.25 cm2.
For now, I will simply continue to advise patients that, happily, this is the case!
Mr Mark Phillips
Consultant Hand Surgeon
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