Repetitive strain injuries

Repetitive strain injuries

THE LANCET and colleagues2 applied standard scientific criteria, such as strength of association, specificity, temporality, consistency, biological p...

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THE LANCET

and colleagues2 applied standard scientific criteria, such as strength of association, specificity, temporality, consistency, biological plausibility, dose-response, as well as consideration of confounders, and concluded that there is an association between various musculoskeletal disorders and workrelated factors. Moreover, much progress has been made in the development of interventions to decrease the incidence and severity of these disorders. Thus, the only barrier to progress seems to be the attitude of those who prefer to divert attention from the preventable aetiological basis for these conditions. Is repetitive strain injury a misleading term? Several terms exist to describe this collection of disorders. I have no objection to the term work-related upper limb disorder, although repetitive strain injury is still used more commonly. I find the word disorder to be more emotive than injury, because it has a more endogenous connotation and can obscure the external factors that precipitate the condition, although perhaps not the associated disability. As noted, repetitive strain injury is not a diagnosis but an umbrella term for various disorders, some of which are easier to diagnose than others. Certainly, clinicians disagree about the existence of some of these diagnoses, let alone their pathophysiological basis. As for carpal tunnel syndrome, the physical examination and symptom pattern are highly predictive. Katz and colleagues3 found the combination of a positive Tinel’s sign and a classic hand pain diagram to have a specificity of 89%, a positive predictive value of 71%, and a negative predictive value of 69% in a high-prevalence population. They also reported a high degree of accuracy with which experienced neurologists can identify carpal tunnel syndrome solely on the basis of signs and symptoms (positive predictive value 65%, negative predictive value 87%). Stevens and colleagues4 found that 73% of hands clinically diagnosed had positive electromyographic findings. Domestic and work-related factors are important. Indeed, I listed several effective psychosocial interventions at the workplace. Excessive physical or psychosocial stresses at work will affect the home environment, and vice versa. Although it is crucial to address nonwork-related physical and psychosocial factors, the inappropriate focus on a worker’s domestic situation may create unnecessary antagonism if the worker attempts to introduce changes at the workplace. In most cases, workers faced with excessive demands generally try to cope with their painful backs and limbs on the job, preferring not to jeopardise their position by calling attention to their condition.

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I find it disheartening to read Helliwell’s assertion that the only effective intervention is psychosocial. I cited only review articles because the number of reports of successful interventions is too lengthy to list. I refer Helliwell to the numerous articles that make up entire journals, such as Ergonomics and Applied Ergonomics. Clinicians must understand that the physical and psychosocial characteristics of work (and nonworkplace settings) can profoundly affect their patients’ wellbeing and produce various musculoskeletal disorders. Physicians have a crucial role in the early recognition of these disorders and in stimulating appropriate ergonomic interventions to reduce their frequency and severity.

strain injury.4 Indeed, the term repetitive strain injury has been repeatedly challenged because of its inaccuracy and the potential for medical iatrogenesis. It would have been more appropriate to separate the various well-described soft-tissue injuries from repetitive strain injury and to discuss their aetiology, pathophysiology, and subsequent treatment than to conflate these two concepts.

Annalee Yassi

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E Michael Shanahan Depar tment of Medicine, Flinders Medical Centre, Bedford Park, South Australia 5042

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Occupational and Environmental Health Unit, University of Manitoba, Winnipeg, Manitoba, Canada R3E OW3

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Silverstein MA, Silverstein BA, Franklin GM. Evidence for work-related musculoskeletal disorders: a scientific counter argument. J Occup Environ Med 1996; 38: 477–84. Hagberg M, Silverstein B, Wells R, et al. In: Kuorinka I, Forcier L, eds. Work related musculoskeletal disorders (WRMSDs): a reference book for prevention. London: Taylor and Francis, 1995: 5–184. Katz JN, Larson MG, Sabra A, et al. The carpal tunnel syndrome: diagnostic utility of the history and physical examination findings. Ann Intern Med 1990; 112: 321–27. Stevens JC, Sun S, Beard CM, O’Fallon WM, Kurland LT. Carpal tunnel syndrome in Rochester, Minnesota, 1961–1980. Neurology 1988; 38: 134–38.

SIR—Yassi1 describes repetitive strain injury as “an umbrella term for disorders that develop as a result of repetitive movements, awkward posture, and force”. However, this definition is generally not used in Australia or other countries.2 In Australia, repetitive strain injury has generally come to mean chronic upper limb pain that is not related to welldefined localised entities, the pathophysiology of which is unclear and controversial. To suggest, as Yassi does, that Australian sceptics argued that repetitive strain injuries (including well-defined medical conditions) were conversion disorders or a product of economic incentives and social iatrogenesis is to misunderstand the debate, which was not about the welldefined medical conditions that seem to be the focus of her article. This debate has centred around the contributions of neuropathological,3 psychological, biomechanical, and sociopolitical3 aetiologies of chronic upper limb pain. Furthermore, the treatment strategies and staging categories put forward by Yassi are inappropriate for what is generally regarded as repetitive

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Yassi A. Repetitive strain injuries. Lancet 1997; 349: 943–47. Diwaker HN. What do doctors mean by tenosynovitis and repetitive strain injury? Occup Med 1995; 45; 97–104. Cohen ML, Arroyo JF, Champion GD, Browne CD. In search of the pathogenesis of refractory cervicobrachial pain syndrome: a deconstruction of the RSI phenomenon. Med J Aust 1992; 156: 432–36. Cleland LG. “RSI”: a model of social iatrogenesis. Med J Aust 1987; 146: 236–39. Ferguson DA. “RSI”: putting the epidemic to rest. Med J Aust 1987; 147: 213–14.

SIR—We welcome The Lancet’s initiative in commissioning a series on occupational medicine.1 The choice of work-related musculoskeletal disorders from the first article reflects the common occurrence of these conditions.2,3 However, we are surprised that Yassi4 uses the term “repetitive strain injuries” as an umbrella term to cover a whole range of work-related musculoskeletal disorders. There is little adequate epidemiological evidence of the importance of repetition, force, and posture for each of the various disorders covered by this term and for some, even the pathological basis for so-called injury. We agree with Yassi that the use of differing terminology and lack of clear case definitions have impeded the critical evaluation of these conditions. We recently held a combined Delphi exercise consensus conference in the UK for the Health and Safety Executive to see whether diagnostic criteria could be agreed across various professional interests (eg, rheumatology, orthopaedic surgery, occupational medicine, physiotherapy) in one country. We were able to agree diagnostic criteria for such well-defined clinical entities as carpal tunnel syndrome, tenosynovitis of the wrist, and shoulder capsulitis. But we were left with a condition that we labelled “pain in the forearm in the absence of specific diagnosis or pathology”. This might seem an unsatisfactory alternative to repetitive strain injury, but it does reflect the current state of knowledge and accepts that forearm pain not associated with any specific

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anatomical structure is a real entity, is associated with considerable morbidity, and requires further epidemiological and ergonomic investigation.

be influenced by nutritional treatment. Food may after all be a simpler, cheaper, and more well-established means of achieving the same effects.

*J M Harrington, D Gomper tz, R H McCaig

R V Heatley

*Institute for Occupational Health, University of Birmingham, Birmingham B15 2TT, UK; and Health and Safety Executive, Bootle, UK

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Frankel DH. Occupational medicine octet. Lancet 1997; 349: 896. Hodgson JT, Jones JR, Elliot RC, Osman J. Self-reported work-related illness, research paper 33. Sudbury, Suffolk: HSE Books, 1993. Kuorinka I, Hagberg M, Silverstein B, et al. Work related musculoskeletal disorders (WMSDS): a reference for prevention. London: Taylor and Francis, 1994. Yassi A. Repetitive strain injuries. Lancet 1997; 349: 943–47.

Division of Clinical Medicine, School of Medicine, St James’s University Hospital, Leeds LS9 7TF, UK

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Nutritional replenishment as an alternative to TNF- in Crohn’s disease SIR—It is widely accepted that in active inflammatory bowel disease the concentrations of many peripheral blood cytokines are increased. This includes tumour necrosis factor- (TNF-) in Crohn’s disease and ulcerative colitis.1 This observation has led to the therapeutic use of antibodies to TNF- in Crohn’s disease.2 This cytokine has a diverse range of actions, and it has been suggested that its chronic elevation, as occurs in active inflammatory bowel disease, may be a factor contributing to the anorexia and growth failure commonly associated with Crohn’s disease.3 Cytokines, including TNF-, are known to have the direct effects of suppressing the appetite centre of the central nervous system, and inhibiting gastric emptying. Nutritional depletion in itself has been shown to be associated with several of the immunological abnormalities present in active Crohn’s disease.4 Nutritional treatment has also been shown to be equally effective in treating acute attacks of Crohn’s disease as anti-inflammatory corticosteroid therapy, the clinical improvement being associated with striking lowering of previously raised soluble interleukin-2 receptor level in peripheral blood which is usually associated with active disease and is a sensitive marker of disease activity.5 The therapeutic benefits of genetically engineered antibody to TNF- in Crohn’s disease may be effected by similar mechanisms to those occurring in nutritional replenishment. Further studies should take this into account and monitor other immunological indices known to

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Dalton HR, Heatley RV. Inflammatory bowel disease. In: Heatley RV, ed. Gastrointestinal and hepatic immunology. Cambridge: Cambridge University Press, 1994: 114–46. Stack WA, Mann SD, Roy AJ, et al. Randomised controlled trial of CDP571 antibody to tumour necrosis factor- in Crohn’s disease. Lancet 1997; 349: 521–24. MacDonald TT, Hutchings P, Chey MY, Murch S, Cooke A. Tumour necrosis factoralpha and interferon-gamma production measured at the single cell level in normal and inflamed human intestine. Clin Exp Immunol 1990; 81: 301–05. Harries AD, Danis VA, Heatley RV. Influence of nutritional status on immune functions in patients with Crohn’s disease. Gut 1984; 25: 465–72. Duane PD, Teahon K, Crabtree JE, Levi AJ, Heatley RV, Bjamason I. The relationship between nutritional status and serum soluble interleukin-2 receptor concentrations in patients with Crohn’s disease treated with elemental diet. Clin Nutr 1991; 10: 222–27.

Infection and childhood leukaemia near nuclear sites SIR—Inskip’s commentary (April 5, p 969)1 on childhood leukaemia near nuclear sites in the UK, notably Sellafield and Dounreay, could have taken further the question of an infective aetiology. It was the high rate of childhood leukaemia at these sites that led to the population mixing (infective) hypothesis that holds that the bringing together of rural and urban groups, or different socioeconomic groups, can increase the frequency of childhood leukaemia through increased contact between susceptible and infected individuals. A high proportion of susceptible individuals is important for an epidemic. Geographical isolation, high social class, and frequent population turnover all promote susceptibility. Seascale is unique in these respects: a cul-de-sac in an already isolated area, it has the highest proportion of social class I of any comparable rural parish, and an unusually high population turnover, thereby maintaining a large number of susceptible children. A nearby source of infection is also present: Sellafield has the largest rural industrial workforce in the UK and also, for 45 years, a large number of mobile construction workers.2,3 Inskip overlooks these factors and, mentioning only the original population

influx, invokes an “elusive Seascale factor”. Inskip states that “there are limits to what can be deduced” given the small number of cases of childhood leukaemia in Seascale and near Dounreay. But the number of cases in a hypothesis-generating observation is irrelevant; the findings in studies testing that hypothesis in other populations are crucial. The population-mixing hypothesis has now been supported by 11 studies in the UK, Greece, and Hong Kong, thereby explaining more than 200 excess cases of childhood leukaemia.2–4 The greater excess of cases in Seascale than in these studies conceals a misleading inconsistency. Thus, Inskip correctly refers to the Dounreay area but only to Seascale in relation to Sellafield, though this parish is the southeast segment of Sellafield’s immediate vicinity. Restricting attention to Seascale in this way maximises the excess, but results in bias. Cases in this community were revealed when a television team investigated health aspects connected with Sellafield, which lies outside Seascale parish where the cases occurred. To underline the pitfall of allowing these observations to determine the focus of investigation instead of the putative cause—ie, Sellafield—the analogy has been used of the Texas sharpshooter who first fires his gun and then draws the target round the bullethole.5 The whole of the immediate vicinity of Sellafield should also be studied. When this approach was used,3 the excess was similar to that reported in other studies of rural population mixing2 which also include small areas with an incidence of childhood leukaemia similar to that in Seascale.4 Infection is further supported by differences in age between individuals who are born locally and incomers, suggesting early immunising effects among the former, as noted in Burkitt’s lymphoma.2 Overall, the evidence is consistent with infection. L J Kinlen Cancer Research Campaign, Epidemiology Unit, Depar tment of Public Health and Primar y Care, University of Ox ford, Radcliffe Infirmar y, Ox ford OX 2 6HE, UK

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Inskip H. Childhood leukaemia near nuclear sites re-examined. Lancet 1997; 349: 969–70. Kinlen LJ. Epidemiological evidence for an infective basis in childhood leukaemia. Br J Cancer 1995; 71: 1–5. Kinlen LJ, Dickson M, Stiller CA. Childhood leukaemia and non-Hodgkin’s lymphoma near large rural construction sites, with a comparison with Sellafield nuclear site. BMJ 1995; 310: 763–68. Kinlen LJ, Craft AW, Parker L. The excess of childhood leukaemia near Sellafield: a commentary on the fourth COMARE report. J Radiol Protect 1997; 17: 63–71. Olsen SF, Martuzzi M, Elliott P. Cluster analysis and disease mapping—why, when, and how? A step by step guide. BMJ 1996; 313: 863–66.

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