Academic Unit of Musculoskeletal Disease, University of Leeds, Leeds, UK
Correspondence to: Chapel Allerton Hospital, Chapeltown Road, Leeds LS7 4SA, UK. E-mail: Howard.Bird{at}leedsth.nhs.uk
Work-related upper limb disorder (WRULD) remains an enigma [1]. Many rheumatologists attest to the occurrence of symptoms involving various parts of the arm, particularly the hands, wrist and forearm, as a result of overexertion in the workplace, based upon their clinical experience. Orthopaedic surgeons are less convinced, possibly because they see fewer follow-up patients. Often a clearly defined medical symptom is present on both history and examination. Examples are tenosynovitis, epicondylitis and carpal tunnel syndrome. Some have argued forcefully that such specific conditions can be caused by work [2]; others have taken a more balanced viewpoint [3]. Orthopaedic surgeons often argue that such conditions are invariably constitutional, only aggravated rather than caused by the workplace.
Even when such specific conditions are teased apart, a group of patients remain in whom the symptoms are less specific and more diffuse but in whom there is still a strong clinical impression that the condition would not exist were it not for overexertion in the workplace [4]. Originally termed repetitive strain injury (RSI) and reaching epidemic proportions in Australia [5], this term soon fell into disrepute since the word injury already implied blame. Repetitive strain disorder (RSD) was coined, to be replaced by WRULD and, in turn, by local regional pain syndrome. However much the nomenclature was thereby improved, all these variations simply sidestepped the basic problem, which was that the pathology, at least in rheumatological terms, still awaited definition.
Perhaps the scientific speciality of rheumatology sets too high a standard. That athletes should experience similar symptoms at the parts of the body that are overused in their respective sports has caused much less controversy and overuse syndromes have been accepted, diagnosed and treated, normally just by avoidance of the precipitating activity, for decades [6, 7]. Microtrauma, perhaps subclinical haemorrhage into muscles, lactic acid acidosis and even very mild variants of algodystrophy, have all in turn been suggested as possible causes. So have compartment syndromes, the phenomenon where overuse of a muscle leads to raised pressure in an unyielding osteofascial compartment [8]. This respectable surgical diagnosis constitutes a potential orthopaedic emergency since, if left unattended, the increased pressure can lead to muscle necrosis. The syndrome is most recognized in the leg, where it can mimic deep venous thrombosis [9]. Athletes and dancers [10] live in dread of milder forms of this syndrome, colloquially referring to it as shin splints.
On page 1442 of this issue, Pritchard and colleagues follow an interesting clinical trail through which they suggest that mild degrees of compartment syndrome may well account for a proportion of patients with WRULD who present to rheumatologists [11]. Although they imply that this breaks new ground, this is not quite true. Such a phenomenon is already established [1216], though sometimes in journals not always frequented by rheumatologists. In almost all cases, it invariably follows a heavy load. The condition is sometimes initially misdiagnosed [12] or occurs in a highly specific occupation, such as that of a racing cyclist [13]. Recent reports have linked it to more modest activities such as just lifting a heavy load [16].
Pritchard and colleagues review 30 patients who complained of a long duration of diffuse forearm pain of sufficient severity to prevent them carrying on with their normal employment. Twenty-four were female and all additionally fulfilled further criteria for a chronic compartment syndrome, other diagnoses that might also cause forearm pain excluded on clinical grounds. Patients proceeded to measurement of pressure inside the extensor muscle compartment of the forearm at rest and after a 2-min repetitive gripping exercise using an electronic pressure-sensitive probe. Over half the complainants showed a raised compartment pressure at rest, which increased further with repetitive gripping. This also caused pain. Eleven patients with persistently raised pressure were invited to undergo fasciotomy. This was said to not only relieve symptoms but also to relieve pressure. The authors further speculate that other conditions such as radial tunnel compression and posterior interosseus nerve syndrome might in large part be due to compartment syndrome as well.
Intriguingly, the authors also note persistent neuropathic pain of significant severity in one-third of patients on whom decompression has been performed and present in even more that mimic a reflex sympathetic dystrophy, sometimes with vasomotor changes and cold sensitivity. In turn, this new problem once again compromises work capacity, now with an alternative pathology (though the authors argue that these may be overlapping conditions). It remains a possibility that even if the splitting of the fascia does not heal, long-term treatment with intralesional steroid or even gabapentin may yet be required.
Unfortunately, there are some pitfalls typical of the difficulty of working in this area. The study is essentially uncontrolled, the group of patients studied already quite highly selected by referral to a hospital clinic. However, the investigators themselves volunteered as subjects for the testing of the method, providing some evidence of normal values (unless the weight of case notes in this hospital is particularly heavy!) and the successive readings in the subjects who proceeded to operation provide an element of control within the subject group. In some subjects the other asymptomatic arm was measured for comparison, though this was not a consistent requirement in the protocol. There is also a paucity of information on the reproducibility of this particular method, on whether pressure studies are age-related or subject to diurnal variation, and whether either of these might have influenced the results. Ultimately, a more formal case-controlled study will be required, though the findings of this initial compilation of patients are intriguing and strongly suggestive. For the present, the authors maintain a sense of caution in their conclusions, though further work is certainly indicated by these preliminary results. At present only a small number of orthopaedic surgeons and rheumatologists have access to pressure measurement [3]. Perhaps its use deserves to be more frequenteven part of a core curriculum.
It is also of note that a proportion of these patients were referred not by their general practitioners but by lawyers in connection with claims for compensation for work-related injury. For such claims to be successful, the judge has to be satisfied that a discrete medical condition exists, that it was caused entirely by the work and that this should have been foreseen by management [4]. Frequently the case does not succeed on one of the first two of these counts, experts for the defendants (invariably an insurance company) arguing that, even if a discreet diagnosis such as epicondylitis or tenosynovitis is proven, this simply represents aggravation of a constitutional problem. The gradient of success becomes steeper if the diagnosis relied upon is merely a WRULD of imprecise cause. Although enlightened judges [1] have recently argued that, even if science is at present too imprecise to confirm the presence of a condition, this does not prevent it from existing, other judges have considered that the evidence presented for a syndrome's existence has been reminiscent of medieval theology. Against this background, Pritchard and colleagues have provided a significant service in postulating and largely defining a hitherto unsuspected contributory factor.
The authors have declared no conflicts of interest.
References
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