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June.) Erythromelalgia induced by nicardipine. SIR,-Dr J P H Drenth contests our report of erythromelalgia associated with nicardipine.'2 He states that there is a ...
At one point they correctly state that the magnitude of critical difference necessary to indicate a change in the patient's condition is related to the probability level selected. The implication should be that this probability level, like the magnitude of change, can legitimately change according to clinical circumstances, but the authors find that diet has not helped a patient whose cholesterol level fell from 7 62 to 6 49 mmolUl on the ground that this change is not significant at the 0-05 probability level. This patient might be happy to continue dieting so long as the chance that this is helping exceeds 80%, the significance level often selected in randomised controlled trials with individual patients.2 R J LILFORD

Department of Obstetrics and Gynaecology, St James's University Hospital, Leeds LS9 7TF I Fraser CG, Fogarty Y. Interpreting laboratory results. Br MedJ 1989;298:1659-61. (24 June.) 2 Guyatt GH, Sackett D, Taylor DW, Chong J, Roberts R, Pugsley S. Determining optimal therapy -randomised trials in individual patients. N Engl3r Med 1986;314:889-92.

Clouds over witnesses SIR,-I have had no opportunity to read Expert Evidence: Interpreting Science in the Law, ' but if Mr Richard Ough's review is accurate the Home Office Forensic Science Service has been misrepresented. The reviewer refers to page 74 in these terms: "we are informed that after the evidence of a forensic scientist (who was perhaps overzealous) was discredited a large scale reorganisation of line management within the Forensic Science Service was performed and new quality control procedures instituted." This statement is incorrect. Concern over the scientific evidence in the case arose directly from quality assurance procedures already in place. I share Mr Ough's view that academic analysis of jurisprudential aspects of expert evidence is timely. I would add that the process is helped if the information used to make the case is accurate. JANET THOMPSON Forensic Science Service, London SW I P 2AW 1 Ough R. Clouds over witnesses. BrMedj7 1989;298:1726-7. (24 June.)

Erythromelalgia induced by nicardipine SIR,-Dr J P H Drenth contests our report of erythromelalgia associated with nicardipine.' 2 He states that there is a causal connection between thrombocythaemia and erythromelalgia, citing the works of Michiels et al,' and reasons that since our patient did not have thrombocythaemia she could not have had erythromelalgia.

Certainly, some patients with thrombocythaemia complain of a disorder which resembles erythromelalgia, as first described by Mitchell in 18784 and characterised by Brown in 1932 on clinical criteria.5 There are, however, many cases that are indistinguishable clinically from thrombocythaemia related erythromelalgia but do not have any platelet dysfunction and for which a causal relation with platelet disorders is untenable-for example, erythromelalgia related to lupus erythematosus, to drugs (such as nifedipine or bromocriptine, in addition to our case with nicardipine), or even to no apparent cause.6 Smith and Allen,7 and others since, divided erythromelalgia into two forms: primitive erythromelalgia (no cause found, usually young patients, sometimes non-responsive to aspirin) and secondary erythromelalgia, especially that secondary to myeloproliferative disorders (thrombocythaemia,

BMJ

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polycythaemia) or to lupus or drugs. In the latter cases the prognosis, treatment, and evolution depend on the underlying disease. Michiels et al found erythromelalgia in 26 of 40 patients with myeloproliferative disorders but did not study the number with myeloproliferative disorders in a population of patients with erythromelalgia.3 They found histological lesions of the microvasculature and suggested that the presence of platelet abnormality with resulting microvascular lesions was necessary for diagnosing erythromelalgia, thereby refuting all other cases of erythromelalgia not associated with abnormal platelets or microvascular disorders." Other authors also found the same microvascular disorders in myeloproliferative disorders as Michiels et al, but without symptoms of erythromelalgia.9 Erythromelalgia is primarily a clinical diagnosis, referring to a syndrome which may have several causes, and it would be wrong to include the presence of a cause as a diagnostic criterion for the disease and then use this to say it is the only cause. We could decide that thrombocythaemia linked erythromelalgia is the true erythromelalgia, and all the rest, though clinically indistinguishable, erythromelalgia-like eruptions-or, alternatively, that primitive erythromelalgia is the only true erythromelalgia and that all secondary cases are erythromelalgia like. This should be done only after careful case-control studies. In any event our case is clinically indistinguishable from erythromelalgia; it fulfils all the criteria for the disease suggested by Lazareth et al,6 except for sensitivity to aspirin: unfortunately we stopped nicardipine (and resolved the problem) before testing the effects of aspirin, and so do not have that criterion. As for the assertion that nicardipine could not possibly cause erythromelalgia because it has antiplatelet properties, this rests on the assumption that there is no erythromelalgia without platelet disorders. Nifedipine has the same properties as nicardipine and has also been suspected of causing erythromelalgia. In our case the time course of the disease, and the exclusion of other causes, favoured nicardipine being the cause. Incidentally, we recently saw a similar case in which a patient had intense, paroxysmal burning pain of the hands the night after starting misoprostol, a prostaglandin E1 analogue (the patient also reported swollen hands but since it was dark did not know if they were red). The symptoms recurred the next night and subsided immediately after misoprostol was stopped, two days later; she refused rechallenge. Clinical examination, blood tests, capillaroscopy, and tests for antinuclear antibodies all gave normal results. She had no thrombocythaemia. This could be related to Jorgensen et al's observations of a hvnersensitivity to prostaglandins in primitive erythromelalgia."' Like the calcium antagonists, prostaglandin analogues are also used in the treatment of Raynaud's phenomenon. H LEVESQUE N MOORE

CHU de Rouen, H6pital de Boisguillaume, 76233 Boisguillaume, France 1 Drenth JPH. Erythromelalgia induced by nicardipine. BrMedI 1989;298:1582. (10 June.) 2 Lesesque H, Moore N, Wolf LM, Courtois H. Erythromelalgia induced by nicardipine (inverse Raynaud's phenomenon?). BrMed.7 1989;298:1252-3. (6 May.) 3 Mtichiels Jj, Abels J, Steketee J, Van Vilet HHDM, Vuzevski VD. Erythromelalgia caused by platelet mediated arteriolar inflammation and thrombosis in thrombocythemia. Ann Intern Afled 1985;102:466-71. 4 Mitchell SW. On a rare vasomotor neurosis of the extremities and on the maladies with which it may be confounded. Amj MedSci 1878;76:2-36. 5 Brown GF. Erythromelalgia and other disturbance of the extremities accompanied by vasodilatation and burning. Amy Med Sci 1932;183:468-85. 6 Iazareth I, Fiessinger JN, Priollet P. Lerythermalgie, un acrosyvndrome rare. Presse Med 1988;17:2235-9. 7 Smith LA, Allen EV. Erythermalgia (erythromelalgia) of the extremities: a syndrome characterized by redness, heat and pain. Am HcartJ 1938;16:175-88.

8 Priollet P, Bruneval P, Lazareth I. Ervthromelalgia without arteriolar changes. Ann Intern Med 1985;103:639. 9 Amblard P, Leques B, Seigneurin D, Verdaguer S, Reymond JL. Manifestations cutanees des thrombocytc6nies. Ann Dermatol Venereol 1977;104: 115-20. 10 Jorgensen HP, Sandergaard J. Pathogenesis of erythromelalgia. Ach Dermatol 1978;114:112-4. 11 Rademaker M, Cooke ED, Almond NE, et al. Comparison of intravenous infusion of iloprost and oral nifedipinc in treatment of Ravnaud's phenomenon inpatients with systemic sclerosis: a double-blind randomized studv. Br Med J 1989;298:561-4.

Funds for treatment SIR,-I am surprised that Dr R Gabriel' has not followed the example of other hospital specialists who want to treat their patients with expensive drugs which the hospital budget cannot afford. They ask the patient's general practitioner to prescribe. I have no patients receiving dialysis, but I do have one with growth hormone deficiency. At the request of his paediatrician I prescribe 30 ampoules of recombinant growth hormone (Genotropin) per month, a cost of about £ II 000 a year. This distorts my prescribing costs, which worries me not one bit. As I do not intend to be a budget holder I can continue to prescribe this drug and would be prepared to prescribe erythropoietin if I had any patients who needed it. Indeed I can see little difference between the two cases. JOHN M JUSTICE

South Harrow, Middlesex HA2 8RS I Gabriel R. Wanted: funds for a treatment that really works. BrMedJ 1989;299:64. (I July.)

Surgeons and trauma care SIR,-Professor D Trunkey's assertion that the general surgeon should be the central focus of trauma care in Britain' is not rational. Deficiencies in the present system of trauma management in this country have recently been highlighted,2 and it is now clear that placing seriously injured patients in the care of inexperienced casualty officers is unacceptable. The immediate management of victims of major trauma, however, has little to do with operative surgery. Several failings have been shown to reduce survival after trauma, including delayed or nonexistent surgical intervention.' When definitive surgery has been rapidly undertaken mortality has been reduced.4 This presumably explains the calls for such cases to be managed by surgeons. But delay is not inevitable simply because the resuscitation is being carried out by someone other than the surgeon who is to operate on the patient. Quite possibly the reverse could be true. Senior surgeons spend very little time in the accident and emergency department and are infrequently involved in the acute management of trauma. Though the general surgeon will be familiar with the later phases of trauma care this does not necessarily imply competence in its emergency treatment. The various problems associated with severe injury require an appreciation of the pathophysiology of shock and an ability to manage the airway, prevent hypoxia, and restore circulating volume. Few senior general surgeons are comfortable with these requirements and fewer still with other potential problems such as cardiac arrhythmias and cardiopulmonary arrest after trauma.

Severely injured patients should be received in the accident and emergency department, at whatever time of day and night, by a team led by a senior doctor who is experienced in life support after trauma.6 Many patients will require an urgent surgical opinion and possibly urgent surgery. 323