Volume 167 Issue 4

A high incidence of melanoma found in patients with multiple dysplastic naevi by photographic surveillance John W Kelly, Josephine M Yeatman, Cheryl Regalia, Grahame Mason and Amanda P Henham Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au/>". Abstract - Introduction - Methods - Results - Discussion - References - Authors' details - - ©MJA1997 Abstract Objectives: (1) To assess the incidence of melanoma in a cohort of patients with dysplastic melanocytic naevi (DMN) and the relationships between incident melanomas and preexisting naevi and between melanoma risk and numbers of DMN. (2) To examine the role of the patient versus the physician in detecting melanoma and the relative value of surveillance versus prophylactic excision. Design: Prospective cohort study. Patients and setting: Two hundred and seventy-eight adults, each with five or more DMN, were followed up for a mean period of 42 months in a private dermatology practice. DMN were clinically diagnosed. Results: Twenty new melanomas were detected in 16 patients, corresponding to an age-adjusted incidence of 1835/100 000 person-years, 46 times the incidence in the general population. Eleven were detected because of changes evident in comparison with baseline photographs and nine were detected by patients or their partners. Thirteen of the 20 melanomas arose as new lesions and only three from DMN. Melanoma risk rose with increasing numbers of DMN. Conclusions: Increasing numbers of DMN are associated with increasing melanoma risk. Surveillance (baseline photography and follow-up) enabled early diagnosis of melanoma and was very much more cost-effective in preventing life-threatening melanoma than prophylactic excision of DMN. MJA 1997; 167: 191-194 Introduction Eight case-control studies have indicated that dysplastic melanocytic naevi (DMN) are a strong and independent risk factor for the development of melanoma.1-8 Cohort studies show that individuals with DMN develop more melanomas than the general population.9-14 Only one cohort study has assessed the association of incident melanomas with preexisting naevi and the role of the patient versus the clinician in detection.10 None has examined an Australian cohort or addressed the relationship between DMN numbers and melanoma risk, the cost-effectiveness of surveillance compared with prophylactic excision or the occurrence of non-melanoma skin cancer in subjects with DMN. We followed a cohort of 278 Australian patients with DMN, using baseline skin surface photography to address these issues. Methods All patients who presented to the private dermatological practice of one of us (J W K) between March 1985 and November 1992 who required total body cutaneous examination were assessed for entry to the study. Any who had five or more clinically determined DMN and who were aged 18 years or more were offered baseline skin surface photography and follow-up on an annual basis. Over 80% had been referred for assessment of their atypical naevi or because of other melanoma risk factors, particularly a personal or family history of melanoma. In November 1993 all patients who had baseline photographs and had returned for at least one 12-month follow-up visit were entered in the study. The entry criterion of five DMN was based on the results of an earlier study that suggested to us that this number of DMN is associated with sufficient melanoma risk to justify entry to a screening program.2 A systematic set of 14 baseline photographs of the skin surface was used. A clinical photographer (A P H) worked with us in designing the views and did the photography, using anatomical site definitions to define standard views of recognisable body regions rather than using standard magnifications (Box 1). This reduced the number of views needed to cover the skin surface while providing adequate magnification. At entry to the study subjects were advised about their high risk of mela noma; three-monthly self-examination was recommended, the clinical features of early melanoma were discussed and appropriate sun protection measures were described. DMN were diagnosed clinically accor ding to published criteria.15 A naevus was considered clinically dysplastic if it had a macular component and showed at least three of the following five clinical features: ill-defined border, irregularly distributed pigmentation, background erythema, size greater than 5 mm, and irregular border. An exact count was made of the number of DMN and recorded in ranges 1-4, 5-10, 11-20, 21-50 and >50. The total number of MN was estimated and recorded in ranges <20, 21-50, 51-100 and 101-500. Patients were reviewed at 6- to 12- month intervals. Total body cutaneous examination was performed at each visit and the patient's pigmented lesions were compared with baseline photographs. Excisional biopsies were performed for any lesions that were clinically suggestive of melanoma and were not done routinely for histological confirmation of the presence of dysplastic naevi. All histo pathological specimens were examined at a single private pathology laboratory. All melanomas arising during the study were reviewed by one pathologist (G M). Melanomas detected at the initial visit were excluded from the analysis. Results The study enrolled 278 patients (162 women and 116 men). Mean age was 37 years (range, 18-67 years). Sixty-five patients (23%) had a family history of melanoma, 54 (19%) had a past history of melanoma, and 9 (3%) had both. None were from melanoma-prone families (as defined by a history of two or more affected first degree relatives). The mean period of follow-up was 42 months (range, 12-99 months). Twenty melanomas were detected in 16 patients over 955 person-years of follow-up. The age-adjusted incidence of melanoma in this group was 1835/100 000 person-years, 46 times the age-adjusted incidence of in-situ and invasive melanoma of 40/100 000 person-years for the population of Victoria in 1990 (G Giles, Anti-Cancer Council of Victoria, 1996, personal communication). The mean time from baseline to diagnosis of melanoma was 36 months (SD, 12 months; range, 11-75 months). Eleven of the 20 melanomas were detected at follow-up visits by comparison with the baseline photographs. These 11 patients were unaware of the changing lesion, and in most of these lesions the change would not have been apparent to the clinician without the use of photo graphs. Seven melanomas were detected by the patient as a change seen on self-examination and two were detected by patients' partners. Four were amelanotic melanomas that did not fulfil the normal diagnostic criteria for melanoma; nonetheless, one of these was detected by the patient. Detecting the 20 melanomas in these 278 patients required 1554 patient consultations (78 for each melanoma). Two hundred and ten biopsies were performed to assess changes observed during follow-up of 104 patients (10 biopsies for each melanoma detected). Not all changes in pigmented lesions led to a biopsy: if melanoma could be confidently ruled out on clinical examination and skin surface microscopy, the lesion was simply rephoto graphed. Histopathological results of these biopsies are shown in Box 3. Changing dysplastic naevi were the predominant source of clinically suspicious change; we do not know how many of these may have progressed to melanoma if they had not been removed. Nineteen non-melanoma skin cancers were detected during follow-up in this group of patients and removed: 16 basal cell carcinomas, one squamous cell carcinoma, one keratoacanthoma, and one Bowen's disease. Of the 16 patients who developed mela noma, five had a family history and seven had a past history of melanoma. Patients with melanoma were more likely to have had a previous melanoma (P = 0.001) and to have a family history of melanoma (P = 0.05) than those who had not. The percentage of patients in each risk group who developed melanoma is shown in Box 2. Boxes 4 and 5 show the incidence of melanoma in the study cohort in relation to the number of dysplastic naevi and total naevi. For an Australian population, the total numbers of naevi were not remarkable (61% had 100 naevi or less), but there were large numbers of DMN (59% had more than 10). Melanoma incidence correlated more closely with increasing numbers of DMN than with increasing total numbers of naevi. Subjects with 21 to 50 DMN developed melanomas at a rate of 3.3% per year. The 20 incident melanomas were all superficial spreading in type. Twelve were invasive and eight were in situ. All the invasive lesions were less than 0.6 mm thick and level II,16 except one amelanotic melanoma that showed a desmoplastic component and invaded to 1 mm in thickness and reached level IV.16 According to the criteria of Clark et al.,17 15 were classified as radial growth phase lesions and four as vertical growth phase; one was classified separately as desmoplastic. The melanomas were widely scattered over the skin surface, with six on the upper limbs, four on the upper back, four on the lower limbs, three on the chest, two on the abdomen, and one on the head. Seven melanomas showed histological evidence of an associated benign naevus (intradermal naevoid remnants in four and features of dysplastic naevi in three). Nine melanomas evolved as a change in a preexisting pigmented lesion that had been evident on baseline photos. In two of these nine the preexisting pigmented lesion was likely to have been a de novo melanoma. One of these patients had a stable pigmented lesion on the right side of her chest over six years. It was excised when it began to enlarge and darken and was found to be a level II, 0.6 mm thick melanoma without histological evidence of any associated naevus. A second patient had a tiny, 2 mm diameter lesion on his chest at his first visit. At his initial review visit, six months later, this had enlarged slightly and become more angular in shape. Histologically, this was a level I melanoma with no associated naevus. Discussion In this study the presence of five or more clinically determined DMN identified a group of patients with 46 times the general population incidence of melanoma. None of these patients came from melanoma-prone families, in whom Clark et al. originally described dysplastic naevi.18 Five cohort studies of patients with DMN who are not from melanoma-prone families have been published and all showed a very high rate of mela noma.9-13 These findings confirm those from case-control studies showing that DMN constitute a strong and independent risk factor for melanoma.1-8 Our age-adjusted incidence of mela noma of 1835/100 000 person-years is higher than that reported in other studies (692-709/100 000 person-years).9,11 This may be explained by the relatively large numbers of DMN in our patients (Box 4) and by the higher background rate of melanoma in Austra lia than in the United States and United Kingdom. We did not examine a cohort of control patients, but Marghoob et al. did.12 They found a 10-year cumulative risk of melanoma of 10.7% among 287 patients with at least one large naevus, one atypical naevus and 100 total naevi. This risk compared with a 0.62% 10-year risk among 831 controls selected from patients requiring annual dermatological follow-up for other reasons. We have intentionally continued to use the word "dysplastic" rather than "atypical". These naevi have been studied because they are believed to be associated with melanoma risk. There are other naevi that are clinically atypical and that are not linked with melanoma risk. Examples are naevus spilus, blue naevus and halo naevus. We prefer the term "dysplastic" because it clearly does not embrace these other atypical naevi. There are several definitions in the literature for syndromes associated with atypical or dysplastic naevi. One includes patients with a single atypical naevus, a large (>8 mm diameter) naevus and >100 total naevi.12 Another depends on distribution of atypical naevi on the anterior scalp, dorsa of the feet, iris or buttocks.19 DMN have been demonstrated to be independently associated with mela noma risk and are not always associated with large numbers of naevi or naevi in certain locations. We prefer not to include DMN in a syndrome definition but rather to consider them as a continuous numerical variable. There is evidence from this study (Box 2) and from two case-control studies of increasing risk with increasing numbers of DMN.2,11 The risk associated with a single DMN is likely to be small and insufficient to justify our follow-up regimen. It is also difficult to accurately diagnose a single naevus as being dysplastic or otherwise on clinical grounds, but much more easy to identify the patient with numerous DMN. It is also difficult to apply definitions of large numbers of naevi in different geographical locations. A recent Australian study reported a mean total count of naevi (>2 mm diameter) that approached 100 in 15-year-old adolescents, which is considered a large number in the United States and United Kingdom.20 The proportion of the Australian adult population with five or more dysplastic naevi has not been defined. One study of 1123 Australian schoolchildren aged 6-15 years showed that 2.7% had three or more dysplastic naevi according to the clinical definition applied here.21 Two-thirds of the incident melanomas in this study were de novo lesions. This finding is similar to those of studies that examine the histological frequency of associated naevi with melanoma, which suggest that 43%-77% of melanomas are new lesions.22-24 The predominance of de novo melanoma in these patients supports management by photographic surveillance rather than by attempts at prophylactic excision. If every one of the 5838 DMN present in our cohort of patients had been excised at the outset, only three of the incident melanomas would have been prevented. Ninety-three DMN were excised in the course of the study because of changes evident in comparison with photographs and because the possibility of melanoma could not be confidently excluded. These changing DMN would seem to be the most likely pigmented lesions to develop into melanoma, and it is possible that some would have progressed to melanoma had they been left in place. When consultations and biopsies are costed at the Australian Government's Medi care Schedule rates for 1997 and $100.00 is allowed per set of photo graphs, the cost of diagnosing each mela noma in this study is $5583. Prophy lactic excision of all dysplastic naevi would have cost $1118038 and would have prevented only three of 20 mela nomas, at a cost of $395038 each. The use of baseline photographs in patients with many floridly atypical pigmented lesions provided knowledge of the stability of many lesions that would otherwise have demanded excisional biopsy, and greatly reduced the number of excisions needed in managing such patients. Patients commonly presented with concern about a change in a particular pigmented lesion. Reference to the photographs usually revealed no change and the lesion remained under observation. Only 10 biopsies were necessary to detect each melanoma and less than one biopsy was necessary per subject in the course of this study. The melanomas incident in this study were detected at an earlier stage than other melanomas that were incident in the State of Victoria in 1990. In-situ melanomas comprised 45% of those seen in the DMN cohort and 33% of those seen in Victoria for 1990 (G Giles, Anti-Cancer Council of Victoria, 1996, personal communication). Median tumour thickness was 0.40 mm in our cohort and 0.77 mm for the State in 1990. Mean tumour thickness for invasive melanoma in the cohort was 0.44 mm compared with 1.40 mm (95% confidence interval, 1.29-1.51) for the State. It is possible that such close surveillance leads to the detection of some melanomas that would otherwise have remained undetected and may have regressed spontaneously or failed to progress and become life threatening. Such "harvesting" of early melanomas may contribute to the very high incidence observed. We conclude that numerous dysplastic naevi identify patients at high risk of melanoma. Baseline photography of the entire skin surface and 6-12-monthly surveillance provides an effective method for early detection of incident melanomas. As most new melanomas were de novo lesions, prophylactic excision of dysplastic naevi would not have provided a satisfactory alternative to follow-up and does not provide sufficient risk reduction to justify the cost and morbidity of the procedure. References Grulich AE, Bataille V, Swerdlow AJH, et al. Naevi and pigmentary characteristics as risk factors for melanoma in a high-risk population: a case-control study in New South Wales, Australia. Int J Cancer 1996; 67: 485-491. Holly EA, Kelly JW, Shpall SN, et al. Number of melanocytic nevi as a major risk factor for malignant melanoma. J Am Acad Dermatol 1987; 17: 459-468. Swerdlow AJ, English J, MacKie RM, et al. Benign melanocytic naevi as a risk factor for malignant melanoma. BMJ 1986; 292: 1555-1559. Augustsson A, Stierner U, Rosdahl I, et al. Common and dysplastic naevi as risk factors for cutaneous malignant melanoma in a Swedish population. Acta Derm Venereol (Stockh) 1990; 71: 518-524. Halpern AC, Guerry D, Elder DE, et al. Dysplastic nevi as risk markers of sporadic (nonfamilial) melanoma. Arch Dermatol 1991; 127: 995-999. Grob JJ, Gouvernet J, Aymar D, et al. Count of benign melanocytic naevi as a major indicator of risk for nonfamilial nodular and superficial spreading melanoma. Cancer 1990; 66: 387-395. Garbe C, Kruger S, Stadler R, et al. Markers and relative risk in a German population for developing malignant melanoma. Int J Dermatol 1989; 28: 517-523. Roush GC, Nordlund JJ, Forget B, et al. Independence of dysplastic nevi from total nevi in determining risk for nonfamilial melanoma. Preventive Medicine 1988; 17: 273-279. Mackie RM, McHenry P, Hole D. Accelerated detection with prospective surveillance for cutaneous malignant melanoma in high risk groups. Lancet 1993; 3421: 1618-1620. Rivers JK, Kopf A, Vinokur AF, et al. Clinical characteristics of malignant melanomas developing in persons with dysplastic naevi. Cancer 1990; 65: 1232-1236. Halpern AC, Guerry D, Elder DE, et al. A cohort study of melanoma in patients with dysplastic nevi. J Invest Dermatol 1993; 100: 346-349. Marghoob AA, Kopf AW, Bart RS, et al. Risk of cutaneous malignant melanoma in patients with "classic" atypical mole syndrome. Arch Dermatol 1994; 130: 993-998. Kang S, Barnhill RL, Mihm MC, et al. Melanoma risk in individuals with clinically atypical naevi. Arch Dermatol 1994; 130: 999-1001. Schneider JS, Moore DH, Sagebiel RW. Risk factors for melanoma incidence in prospective follow-up. The importance of atypical (dysplastic) nevi. Arch Dermatol 1994; 130: 1002-1007. Kelly JW, Crutcher WA, Sagebiel RW. Clinical diagnosis of dysplastic melanocytic nevi. J Am Acad Dermatol 1986; 14: 1044-1052. Clark WH Jr, From L, Bernadino EH, et al. Histogenesis and biological behaviour of primary human malignant melanoma of the skin. Cancer Res 1969; 29: 705-727. Clark WH, Elder DE, Guerry D, et al. Model predicting survival in stage I melanoma based on tumour progression. J Natl Cancer Inst 1989; 81: 1893-1904. Clark WH, Reimer RR, Greene M. Origin of familial malignant melanomas from heritable melanocytic lesions. Arch Dermatol 1978; 114: 732-738. Newton JA, Bataille V, Griffiths K, et al. How common is the atypical mole syndrome phenotype in apparently sporadic melanoma? J Am Acad Dermatol 1993; 29: 989-996. Kelly JW, Rivers JK, MacLennan R. Sunlight: a major factor associated with the development of melanocytic nevi in Australian school children. J Am Acad Dermatol 1994; 30: 40-48. Rivers JK, Maclennan R, Kelly JW, et al. The Eastern Australian childhood nevus study: prevalence of atypical nevi, congenital nevus-like nevi, and other pigmented lesions. J Am Acad Dermatol 1995; 32: 957-963. Marks R, Dorevitch AP, Mason G. Do all melanomas come from "moles"? A study of the histological association between melanocytic naevi and melanoma. Australas J Dermatol 1990; 31: 77-80. Sagebiel RW. Melanocytic nevi in histologic association with primary cutaneous melanoma of superficial spreading and nodular types: Effect of tumour thickness. J Invest Dermatol 1993; 100 Suppl: 322S-325S. Skender-Kalnenas TM, English DR, Heenan PJ. Benign melanocytic lesions: risk markers or precursors of cutaneous melanoma? J Am Acad Dermatol 1995; 33: 1000-1007. (Received 10 Dec 1996, accepted 10 Jun 1997) Authors' details Victorian Melanoma Service, Alfred Hospital, Melbourne, VIC. John W Kelly, MD BS, FACD, Head; Head of Dermatology Unit, Alfred Hospital; Clinical Associate Professor, Monash University Department of Medicine. Dermatology Unit, Alfred Hospital, Melbourne, VIC. Josephine M Yeatman, MB BS, GradDipEpi, Registrar. Cheryl Regalia, Medical student, University of California at San Diego; now MD. Dorevitch Laboratories, Melbourne Grahame Mason, MB BS, FRCPA, Pathologist. Department of Photography, Northern Territory University, Darwin, NT. Amanda P Henham, BAppSci(Photog), SRN, Lecturer. Reprints: Dr J W Kelly, Victorian Melanoma Service, Alfred Hospital, Commercial Road, Prahran, VIC 3181. ©MJA 1997 <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia.

John W Kelly · Josephine M Yeatman · Cheryl Regalia · Grahame Mason · Amanda P Henham

Notable Case Ephedrine abuse causing acute myocardial infarction Jerome G L Cockings and Michael A Brown "On the street", the more expensive illegal psychostimulants, such as cocaine or amphetamine, may be mixed with or substituted for cheaper drugs such as ephedrine -- with added risk to the user. We report diffuse myocardial injury in a 25-year-old man who presented with pulmonary oedema after intravenously injecting himself with ephedrine, believing it to be amphetamine. MJA 1997; 167: 199-200 Introduction - Clinical record - Discussion - References - Authors' details - - Articles on similar material Introduction The abuse of psychostimulants, such as cocaine and amphetamines, is of concern in Australia -- they are among the most widely used of the illicit drugs after cannabis.1 Occupational use of stimulant drugs is also a problem -- there have been accidents involving heavy transport vehicles whose drivers had taken ephedrine.2 In addition, ephedrine may be taken by "recreational" drug abusers when it is mixed with or substituted for other illicit drugs such as amphetamines. Ephedrine has both cardiovascular and central nervous system effects, but, although the cardiovascular risks of major psychostimulants such as cocaine are well known,3 little has been reported for ephedrine. We report a patient who injected himself intravenously with ephedrine, sustaining diffuse myocardial injury which resolved with inotropic support and ventilation. Clinical record A 25-year-old man with a history of intravenous psychostimulant abuse presented to hospital with progressive dyspnoea two hours after injecting himself intravenously with a solution of a white powder he believed was amphetamine. He had no other medical history of note, was a non-smoker and had previously been well. There was no family history of sudden cardiac death. Serum lipid levels were not measured. On examination he was conscious but tachypnoeic and cyanosed. He was afebrile, tachycardic (pulse, 140 beats/min), normotensive (110/70 mmHg) and hypoxic (Pao2, 49 mmHg), with hypocapnia (Paco2, 33 mmHg), a mild alkalosis (pH, 7.45) and a pronounced leukocytosis (44 x 106 cells/L). He had a reduced cardiac output (2.2 L/min; normal range, 4.5-6.5 L/min), with a pulmonary artery occlusion pressure (an estimate of left atrial pressure) of 30 mmHg. There was bilateral "bat's wing" opacification on chest x-ray, consistent with a clinical diagnosis of pulmonary oedema. Within an hour of admission and treatment with diuretic and oxygen, further deterioration with cardiogenic shock necessitated intubation, ventilation and admission to an intensive care unit. Initially, the lungs were poorly compliant (49 mL/cmH2O; normal range, 70-100 mL/cmH2O) and the alveolar-arterial (A-a) O2 gradient was elevated (260 mmHg; normal range, < 50 mmHg when on 80% O2). He received continuous inotropic support with adrenaline, initially at 38 µg/min, which was steadily reduced over three days. By Day 3, his cardiac output was 5.5 L/min without inotropes. His respiratory function and gas exchange improved steadily and he was extubated on Day 5. Results of microbiological investigations (tracheal aspirate, blood culture and urine culture) were negative and antibiotics were not given. On admission, electrocardiograms revealed widespread ST-segment depression with T-wave inversion, consistent with subendocardial infarction and ischaemia. A posterior infarction could not be excluded. The peak serum creatine kinase (CK) level was 2360 U/L (normal range, 20-130 U/L) (CK-MB isozyme fraction, 6.1%; normally < 2%), with rises in serum levels of aspartate aminotransferase (to 222 U/L [normal range, < 45 U/L]) and lactate dehydrogenase (to 612 U/L [normal range, 110-230 U/L]). A technetium Tc 99m perfusion scan of the myocardium showed mild tracer uptake in the left myocardium and more intense uptake in the posterolateral wall, consistent with diffuse myocardial damage and an acute posterolateral infarction. Echocardiography soon after admission showed severe left ventricular dysfunction in all areas except the apex (which showed near-normal contractility), with a poor overall ejection fraction. There was mild mitral regurgitation with no vegetations. Right ventricular function was normal. On Day 6, mild to moderate impairment of left ventricular function was still present, maximum at the base, with mild ventricular dilatation. The patient continued to improve and was discharged from hospital nine days after admission. Laboratory analysis of the unused white powder identified only ephedrine. On review one month later the patient was symptom-free. The resting electrocardiogram showed non-specific ST-segment and T-wave changes. Exercise testing, carried out according to the Bruce protocol,4 was 13.5 min in duration and limited by fatigue. His peak heart rate was 192 beats/min, with no chest pain or ST-segment or T-wave changes. He attained an estimated oxygen consumption of 49 mL/kg per min (normal range, 50-70 mL/kg per min) and an aerobic capacity of 106% of the predicted value. At two months, echocardiography showed normal left ventricular function but persistent trivial mitral regurgitation with a minor prolapse of the anterior leaflet. The patient was counselled about the health risks (such as the risk of bacterial endocarditis) of continuing to inject illegally obtained drugs. Discussion Our patient presented with diffuse myocardial injury consistent with sympathomimetic abuse -- the agent was identified as ephedrine. He recovered adequately after intensive treatment. The stimulatory central nervous system effects of ephedrine -- increased arousal, restlessness and insomnia -- have been recognised for many years. Preparations of the herb ephedra were used in ancient Chinese medicines, and ephedrine, the active alkaloid, was identified in the late 19th century.5 Ephedrine is a direct agonist of both alpha and beta sympathetic receptors and an indirect adrenoreceptor agonist, causing release of noradrenaline from presynaptic sympathetic nerve terminals. Its cardiovascular effects include tachycardia, increased inotropy, arterial vasoconstriction and hypertension,6 and these are the effects for which it is used therapeutically. Amphetamine and pseudoephedrine have similar actions, although amphetamine has more pronounced central nervous system effects.7 Ephedrine is widely available, but despite the potential for abuse that this creates there are few reports of its cardiovascular risks. Bruno et al. described two cases of intracranial haemorrhage and one of a thalamic infarct following excessive ephedrine ingestion,6 highlighting the potential dangers of non-prescribed self-administration of this drug. Chronic cardiomyopathy was documented after long-term ingestion of ephedrine in a cough mixture.8 Myocardial injury occurred after ephedrine given therapeutically for hypotension during labour,9 and coronary artery spasm leading to myocardial injury has been described with pseudoephedrine ingestion.10 The mechanism of the myocardial injury caused by ephedrine overdose is probably similar to that caused by cocaine -- intense diffuse vasoconstriction of both the coronary and the systemic arterial systems, decreasing myocardial perfusion, increasing afterload, and increasing myocardial oxygen utilisation.3 Although severe hypertension would be expected with ephedrine overdose, and may have been present in our patient soon after the injection of ephedrine, on presentation he had severe acute left ventricular failure with a consequent fall in contractility and blood pressure. This necessitated inotropic support rather than the use of vasodilators. Various other factors may have contributed to the myocardial injury in our patient. There may have been contaminants in the syringe, and the injection of insoluble particulate matter may have caused vascular occlusion. This could have been compounded by catecholamine-enhanced platelet aggregation induced by ephedrine. Further, although no other agents were identified in the remaining unused powder, the original injection may have included another myotoxin. Pre-existing coronary artery disease was unlikely in an otherwise healthy young non-smoker. A coronary angiogram was not performed. Although the leukocytosis was pronounced, this was consistent with the severe physiological stress. Nevertheless, in the absence of any other antecedent events or prior myocardial disease, this case report strongly suggests that the acute myocardial infarction was precipitated by the self-injection of ephedrine. "On the street", small quantities of a cheaper drug such as ephedrine may be mixed with stimulants such as amphetamine. This case illustrates the risks associated with the total substitution of ephedrine and the subsequent injection of what is likely to have been a high dose of this drug. References Australian Social Issues Research 1991. Report on the national campaign against drug abuse. Sydney: Social Issues Household Survey 1985-1991. Canberra: AGPS, 1991. Staysafe Committee of NSW 1992. Staysafe 19: Alcohol and other drugs on NSW roads 1. The problem and countermeasures. Sydney: NSW Parliament, 1992. Goldfrank LR, Hoffman RS. The cardiovascular effects of cocaine. Ann Emerg Med 1991; 20: 165-175. Bruce RA. Exercise testing of patients with coronary artery disease. Principles and normal standards for evaluation. Ann Clin Res 1971; 3: 323-332. Kalix P. The pharmacology of psychoactive alkaloids from Ephedra and Catha. J Enthnopharmacol 1991; 32: 201-208. Bruno A, Nolte KB, Chapin J. Stroke associated with ephedrine use. Neurology 1993; 43: 1313-1316. Gawin FH, Ellinwood EH. Cocaine and other stimulants: actions, abuse and treatment. N Engl J Med 1988; 318: 1173-1182. To LB, Sangster JF, Rampling D, Cammens I. Ephedrine-induced cardiomyopathy. Med J Aust 1980; 2: 35-36. Menegakis NE, Amstey MS. Case report of myocardial infarction in labour. Am J Obstet Gynecol 1991; 165: 1383-1384. Weiner I, Tilkian AG, Palazzolo M. Coronary artery spasm and myocardial infarction in a patient with normal coronary arteries: temporal relationship to pseudo-ephedrine ingestion. Cathet Cardiovasc Diagn 1990; 20: 51-53. (Received 27 Feb, accepted 12 June 1997) Authors' details Royal Adelaide Hospital, Adelaide, SA. Jerome G L Cockings, FFICANZCA, FANZCA, Senior Registrar in Intensive Care; Michael Brown, MD, FRACP, Consultant Cardiologist. Reprints will not be available from the authors. Correspondence: Dr J G L Cockings, Consultant Intensivist, Princess Alexandra Hospital, Ipswich Road, Woolloongabba, Brisbane, QLD 4102. E-mail: J. Cockings@mailbox.uq.edu.au Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/>

Michael A Brown

Health service reform: the perceptions of medical specialists in Australia (New South Wales), the United Kingdom and New Zealand Rod J Perkins, Keith J Petrie, Patrick G Alley, Peter C Barnes, Malcolm M Fisher and Peter J Hatfield For editorial comment see Duckett Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au/>". Abstract - Introduction - Methods - Results - Discussion - Disclaimer of conflict of interest - References - Authors' details - - ©MJA1997 Abstract Objective: To examine the effect of recent healthcare service changes (including significant resource constraint and a greater role for the non-medical manager) in the United Kingdom, Australia and New Zealand on medical specialists' perceptions of their healthcare organisation goals and service delivery, and their enthusiasm for their work. Design: Postal questionnaire survey, answered anonymously. Participants and setting: Medical specialists employed either part- or full-time in two United Kingdom National Health Service Trusts (one acute, one mental health/community service), an Australian Area Health Service and a New Zealand Crown Health Enterprise in 1995. Main outcome measures: Participants' rating of their knowledge of employers' organisational goals, ability to influence management, perceptions of changes in resources and service availability since 1990 and changes in enthusiasm for their work over the past four years. Results: 369 of 521 eligible specialists responded (71%); by country -- United Kingdom, 123/186 (66%); New Zealand, 123/160 (77%); Australia, 123/175 (70%). New Zealand specialists were less aware of their employers' organisational goals and had less congruence between these and their own personal goals than United Kingdom or Australian specialists (P < 0.05). Interest in influencing central management was similar in the three countries, but Australian specialists felt management was less likely to follow their advice compared with United Kingdom specialists (P < 0.05). New Zealand specialists perceived that waiting times for non-urgent patients were currently longer than in 1990 compared to United Kingdom specialists (P = 0.02). In all three countries, inpatient beds were perceived to be less available than in 1990, but less so in New Zealand. The ease of replacing equipment was better in New Zealand than in Australia and the United Kingdom (P = 0.00001). More than 50% of participants in all three countries (183/361; 50.7%) reported that their enthusiasm for their work had decreased in the past four years. Conclusion: The effects of health service reforms seem to have reduced enthusiasm for work among medical specialists in Australia, the United Kingdom and New Zealand. MJA 1997; 167: 201-204 Introduction In recent years, Australia, New Zealand and the United Kingdom have seen major structural changes in the way health services are funded and managed (Box 1), and these changes have altered relationships between doctors and managers.1,2 Whether the new structures deliver better services to populations -- in terms of cost, quality and access -- is currently debated, but little information is available on the impact of these changes on the working lives of specialists in hospital settings.3,4 We set out to determine whether the healthcare changes affected specialists' attitudes towards their work and practice. We assessed their perceptions of their current influence on central management, whether their enthusiasm for involvement in healthcare delivery had changed since the changes were instituted, and whether they believed that availability of resources and services to their patients had changed. Methods Participants In 1995 we mailed questionnaires to 521 specialists (individuals holding College postgraduate qualifications) employed full-time or part-time in two United Kingdom National Health Service Trusts (Salford Royal Hospitals and Newcastle City Health), a New Zealand Crown Health Enterprise (Capital Coast Health, Wellington) and an Australian Area Health Service (staff specialists or visiting medical officers in the Northern Sydney Area Health Service, New South Wales). Specialists from two National Health Service Trusts were surveyed to ensure that all specialties were represented from each country. The questionnaire (to be answered anonymously) was mailed with a covering letter from a senior colleague within their organisation. A second questionnaire was sent to all specialists approximately six weeks after the first (as we did not know who replied to the first mailout, we had to send everyone a second). Questionnaire Participants were asked to rate, on seven-point Likert scales: Their knowledge of their employer's goals, the congruence between what they like doing in their work and what their employer wants them to do, their interest in influencing hospital or service management, and the extent to which their advice is noted or acted upon. The time spent per week in hospital management meetings (from less than one hour to more than six hours), on a scale of less than one hour, one to two hours, two to three hours, etc. Their perception of changes in resource availability and service over the past four years; specifically, waiting time for non-urgent patients, availability of beds, and condition and ease of equipment replacement. They were also asked to rate whether their enthusiasm for their work had increased, stayed the same, or decreased. Open-ended questions (e.g., "If your enthusiasm for your work has changed in the past four years, please state why.") invited the participants to comment on the changes. Statistical analysis The results were analysed using the Statistical Package for the Social Sciences (SPSS) for Windows.5 Non-parametric tests were used to analyse the time spent in management meetings. Differences between specialists in the three countries were assessed using one-way analysis of variance and post-hoc Tukey B tests. Differences in the specialists' enthusiasm for work were evaluated using a contingency table and the chi-squared statistic. Results Three hundred and sixty-nine replies were received after the two mailings (overall response rate, 71%). By country, response rates were: United Kingdom, 123/186 (66.0%), Australia, 123/175 (70%) and New Zealand, 123/160 (77%). Twenty-four percent of the specialists were aged under 40 years, 35% were 40-49, 23% were 50-59 and 19% were 60 years or older. Women made up 19% of the total sample and were equally represented in the three countries (chi-squared = 2.92; df = 3; P = 0.23). There were more full-time specialists in the United Kingdom (56 full-time, 27 part-time) than in New Zealand (33 and 58) and Australia (40 and 47) (chi-squared = 17.53; df = 2; P = 0.0001). Time in management meetings There was no difference between New Zealand and Australian participants in the amount of time spent in meetings about hospital or service matters (median for both, less than one hour per week; Mann-Whitney U test = 6950.5; P = 0.18). United Kingdom specialists spent significantly more time in these meetings (median, one to two hours) compared to either New Zealand (Mann-Whitney U test = 5652.5; P = 0.0007) or Australian specialists (Mann-Whitney U test = 5652.5; P = 0.0007). This effect also held when answers for full-time staff only were examined. Knowledge of organisational goals and influence on management New Zealand specialists were significantly less aware of their health care organisation's goals than specialists in the United Kingdom and Australia, and New Zealand specialists had significantly less congruence between their personal goals and those of the organisation (Box 2). Specialists in the three countries were equally keen to influence management, but Australian participants felt their advice was less likely to be followed. Perceptions of changes in resources and availability of services since 1990 New Zealand specialists felt that waiting time for non-urgent patients was longer than in 1990 compared with their United Kingdom colleagues (Box 3). Beds were perceived to be relatively less available than in 1990 in all three countries, with availability much worse in Australia and the United Kingdom. There was no difference in specialists' perception of equipment condition across countries; most considered this to be fair to moderate. New Zealand specialists felt that equipment replacement was much easier than before 1990 compared with their counterparts in Australia or the United Kingdom. Enthusiasm for work The Figure shows that 50.7% of specialists in the three countries (183 of the 361 who answered the question) reported decreased work enthusiasm over the past four years. The decrease in the United Kingdom was smaller than that in either Australia or New Zealand, but with this size sample no between-country differences were demonstrated (chi-squared = 4.6; df = 2; P = 0.10). Responses to open-ended questions The specialists' comments reflected a divergence between their perceptions of adequate clinical practice and the requirements imposed by the healthcare service reforms (see Box 4). Discussion We found that more than half of hospital specialists in all three countries had decreased enthusiasm for their work in the past four years, coinciding with a greater role of non-medical managers and more restrictions on resources in the secondary (hospital) care sector. The responses to the open-ended questions were consistent with this finding. While all specialists acknowledged resource contraints, in the open-ended questions Australian and New Zealand specialists were more critical of their healthcare organisations than were the United Kingdom specialists. However, the consequent involvement of the United Kingdom specialists may result in a heavy workload: "Sometimes the clinical work and admin work is overwhelming, but on good days it's great. Sometimes I worry if I can keep this level of activity up in the long term" [United Kingdom specialist]. The management structures in the employing organisations are such that specialists in the United Kingdom Trusts, particularly at Salford Royal, seem to be more involved in the organisation and management of their services than are Australian and New Zealand specialists. In this Trust, there were 26 clinical directorates, and more than 30% (26/79) of all specialists were clinical directors; although this position implies extensive involvement in management, the clinical director may not be the manager of the service. A similar organisational structure did not exist in the Northern Sydney Area Health Service. At Capital Coast Health (New Zealand) only one of the three general managers was a medical specialist, and none of the departmental managers were clinicians. This may explain why there appears to be greater enthusiasm for work among the United Kingdom specialists and a greater acceptance of resource difficulties (i.e., although they perceived greater resource difficulties, they did not have less enthusiasm for work than their Australian and New Zealand counterparts). This involvement in management may also explain why United Kingdom specialists spend more time in committee work -- a level of involvement that is significant for their employer. On average, the United Kingdom specialists spent one hour more per week in management meetings than their Australian and New Zealand counterparts, and, given the standard working week of 40 hours, our study would suggest that a United Kingdom Trust employing 120 specialists could expect to receive an additional three full-time-equivalents of time commitment to management issues from those specialists compared with their Australian and New Zealand counterparts. The results of our study show that for many hospital specialists health service reform has come at a "cost" -- a loss of enthusiasm for their work. Specialists' involvement in the management of their hospitals or services seems to be related to higher levels of enthusiasm, even when resource constraints may make it difficult for them to perform their duties properly. Our study suggests that the greater involvement of doctors in management is working to the advantage of the United Kingdom specialists and their employers. This could provide lessons for Australian and New Zealand healthcare systems that have values and structures in common with the organisations employing the Australian and New Zealand specialists in this study. Disclaimer of conflict of interest The authors declare no conflict of interest. References Hunter DJ. Doctors as managers: Poachers turned gamekeepers? Soc Sci Med 1992; 35: 557-566. Scrivens E. The management of clinicians in the National Health Service. Soc Policy Admin 1988; 22: 22-34. Ham C. Health care reform; learning from international experience. Milton Keynes: Open University Press, 1997. Ham C. Reforming the New Zealand health reforms. Big bang gives way to incrementalism as competition is abandoned [editorial]. BMJ 1997; 314: 1844. SPSS: Statistical package for the social sciences for Windows [computer program], version 6.1. Chicago, Ill: SPSS Inc, 1995. (Received 28 Oct 1996, accepted 13 March 1997) Authors' details University of Auckland, Auckland, New Zealand. Rod J Perkins, BDS, MHA, Senior Lecturer in Health Management; Keith J Petrie, MA, PhD, Associate Professor in Health Psychology; Patrick G Alley, MB ChB, FRACS, Associate Professor, Department of Surgery. Royal Salford NHS Trust, Salford, United Kingdom. Peter C Barnes, MB ChB, FRCP, Physician and Clinical Director. Royal North Shore Hospital, Sydney, New South Wales, Australia. Malcolm M Fisher, MD, FFICANZCA, Clinical Professor, University of Sydney. Wellington Hospital, Wellington, New Zealand. Peter J Hatfield, MB ChB, FRACP, Renal Physician. Reprints: Dr R J Perkins, Senior Lecturer in Health Management, University of Auckland, Private Bag 92019, Auckland, New Zealand. E-mail: r.perkins@auckland.ac.nz ©MJA 1997 <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia.

Rod J Perkins · Keith J Petrie · Patrick G Alley · Peter C Barnes · Malcolm M Fisher · Peter J Hatfield

Systematic review of the diagnostic accuracy of dermatoscopy in detecting malignant melanoma Justine Mayer Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au/>". Abstract - Introduction - Methods - Data sources - Study selection and data extraction - Results - Design and validity of selected studies - Results of selected studies - Discussion - Acknowledgements - References - Authors' details - - ©MJA1997 Abstract Objective: To assess the evidence that dermatoscopy improves the accuracy of diagnosis of melanomas in clinical practice. Data sources: MEDLINE 1983-January 1997, EMBASE 1980-1996, and bibliographies of retrieved articles. Study selection and data extraction: Studies selected were original studies with formal methods and results sections comparing diagnostic accuracy of dermatoscopy for malignant melanoma with another clinical method; the criterion standard was excision biopsy with histopathological examination; and accuracy of dermatoscopic diagnosis was determined over a spectrum of stages of melanoma and skin lesions commonly confused with melanoma. Data were extracted by a single observer. Data synthesis: 579 articles were identified; six studies met the inclusion criteria. Positive likelihood ratios for dermatoscopy for diagnosis of melanoma ranged from 2.9 to 10.3. Dermatoscopy had 10%-27% higher sensitivity than clinical diagnosis in the two studies with the most clinically equivocal lesions. However, when sensitivity of clinical diagnosis was more than 84%, sensitivity of dermatoscopy was only slightly higher. One study of dermatologists with no training in dermatoscopy showed a significant decrease in sensitivity. Conclusions: Variability between studies in methods, observers and types of pigmented skin lesions and lack of studies in primary care make generalisation of results difficult. Dermatoscopy appeared not to improve the accuracy of diagnosis enough to alter the clinical management of most pigmented skin lesions. Further research with more explicit methods is needed. MJA 1997; 167: 206-210 Introduction Malignant melanoma is an important cause of morbidity and mortality in Australia. Public health strategies emphasise, in addition to reducing sun exposure, early diagnosis and treatment. It has been claimed that dermatoscopy improves the accuracy of diagnosis of malignant melanomas,1,2 but calls have also been made for a systematic review of the evidence3 (see Box 1 for description of dermatoscopy). An ideal diagnostic test achieves maximum levels of sensitivity and specificity. However, as sensitivity reflects a test's ability to identify individuals with the disease, most clinicians considering the diagnosis of melanoma would prefer a test with high sensitivity. Furthermore, diagnostic tests should be performed only if they have the potential to alter clinical management. For pigmented skin lesions, this means helping decide whether to excise the lesion. This review aimed to identify primary studies that researched the diagnostic accuracy of dermatoscopy compared with clinical diagnosis and to assess their implications for clinical practice. Methods The review followed current recommendations on systematic reviews of the accuracy of diagnostic tests.7,8 Data sources MEDLINE Express (Silverplatter Winspirs) on CD-ROM databases January 1983-January 1997 and Elsevier Science EMBASE Database 1980-1996 were searched. The Medline search was conducted with exploded MeSH headings "melanoma" or "skin neoplasms", combined with "sensitivity and specificity", and with text words "dermoscop*", "dermatoscop*", "skin surface microscop*", "epiluminesc*", or "incident light microscop*". Similar strategies were used to search EMBASE. Study selection and data extraction Abstracts of articles were reviewed by the author for studies that met the selection criteria: Original study with a formal methods and results section comparing the diagnostic accuracy of dermatoscopy for malignant melanoma with another method of clinical diagnosis; Excision biopsy with histopathological examination was the criterion standard; and The accuracy of dermatoscopic diagnosis was determined over a large range of pigmented skin lesions, including a spectrum of stages of melanoma and lesions commonly confused with melanoma. Articles describing studies that appeared to meet the criteria were retrieved for more detailed review (after translation if not in English). Bibliographies of articles retrieved were also checked for articles not listed or incorrectly indexed in MEDLINE or EMBASE. Articles that did not meet the selection criteria included those on the terminology of dermatoscopic techniques, development of criteria for diagnosing pigmented skin lesions, observer error of diagnosis, accuracy of diagnosis of a single type of pigmented skin lesion, and accuracy of digital imaging computer programs. Studies providing data on the sensitivity and specificity of dermatoscopy but with no comparison group were also excluded.9,10 Articles that met the selection criteria were reviewed for study validity and applicability to clinical practice.11 The methods section of each article was checked for explicit mention of the criterion standard of histopathological examination, blinding of observers, spectrum of pigmented skin lesions, study setting, patient demographics, prevalence of melanoma, sample size, intraobserver and interobserver error, and the proportion of pigmented skin lesions in which no dermatoscopic diagnosis could be made. Results Three hundred and thirty-six articles were identified from MEDLINE and 243 from EMBASE. Six articles met the inclusion criteria.4,12-16 All were indexed in MEDLINE and one in EMBASE and all were in English. No further articles meeting the inclusion criteria were found on review of the bibliographies of retrieved articles. Design and validity of selected studies The designs of the six studies are summarised in Box 2. Assessment of the studies' internal and external validity was hampered by lack of information. Only Binder et al.14 provided sufficient details of methods to enable the study to be repeated. All studies were set in specialist dermatology clinics, but none provided further details of the setting (i.e., whether a secondary or tertiary referral centre). They investigated selected groups of pigmented skin lesions, with melanomas comprising 15%-41%, but only one study explicitly stated how lesions were chosen for entry into the study.12 All appeared to include only lesions to be excised because of presumed risk of malignancy or, possibly, patient request. None commented on the suitability of the sample to detect clinically important differences in the diagnostic methods being evaluated, and none provided data on all presenting lesions or followed them up to calculate the true false negative rate. Although all studies used the criterion standard of histopathological examination, none commented on how the histological diagnosis was reached, although pathologists may vary in classifying pigmented skin lesions.24,.25 Only four studies provided objective data on melanoma diameter or Breslow depth.4,12,14,15 Five studies assessed dermatoscopy results in vivo and one, from photographic slides.14 Observers in the in vivo studies were assumed to be blinded to the histopathological results, but it was not apparent that clinical and dermatoscopic diagnoses were independent, despite the importance of history in the diagnosis of malignant lesions. Five studies did not provide the criteria used for clinical diagnosis, and only Binder et al. provided complete details of the method of non-dermatoscopic examination. The diagnostic criteria and method of surface microscopy used differed between the studies. Three studies used handheld monocular dermatoscopes with x 10 magnification,4,13,16 and two studies used binocular stereomicroscopes with magnification up to x 40.12,14 One study used both types of instrument, but did not clearly distinguish their results.15 No study remarked that a skin lesion was unable to be diagnosed by dermatoscopy. Results of selected studies Results of the six studies are shown in Box 2. Five of the studies compared dermatoscopy with clinical diagnosis or diagnosis by microscopy without oil. Likelihood ratios for a positive diagnosis of melanoma by dermatoscopy ranged from 2.9 to 10.3 (meaning that pigmented lesions diagnosed as melanoma by dermatoscopy were 2.9 to 10.3 times morelikely to be melanoma than not). Two studies found that dermatoscopy had higher sensitivity than non-dermatoscopic diagnosis,12,13 one found no difference,15 and one found that dermatoscopy increased sensitivity when performed by experts, but decreased it when performed by dermatologists without training in the technique.14 Pazzini et al. provided insufficient data to calculate sensitivity.16 Nachbar et al.4 compared two forms of dermatoscopy -- with explicit structured diagnostic criteria and without these criteria, but combined with clinical diagnosis. They found that dermatoscopy with structured ABCD criteria19,21 (specific for dermatoscopy and differing from the ABCDE criteria for clinical diagnosis) had higher sensitivity and specificity than dermatoscopy without such criteria. Clinical diagnosis varied widely in sensitivity and specificity between the studies, most likely because the lesions varied in their ease of diagnosis. Observers may also have varied in their ability to make the diagnosis. This variability prevented formal meta-analysis and estimation of a single summary statistic for the diagnostic benefit of dermatoscopy. The studies that provided results for handheld monocular dermatoscopes with x 10 magnification are most relevant to clinical practice.4,13 Cristofolini et al.13 found that dermatoscopy with pattern-analysis criteria had slightly higher sensitivity (88%) and specificity (79%) than clinical diagnosis with ABCDE criteria.18 However, the latter was already highly accurate (sensitivity, 85%; specificity, 75%). Nachbar et al. found that dermatoscopy with structured criteria had higher sensitivity (93% versus 84%) and specificity (91% versus 84%) than without such criteria.4 Interestingly, the studies that showed the greatest improvement in sensitivity for dermatoscopy were those that had the lowest baseline sensitivity for clinical diagnosis. Steiner et al.12 found that dermatoscopy increased sensitivity from 59% to 86% (an increase of 27%) compared to microscopy without oil. Binder et al.14 found dermatoscopy performed by experts increased sensitivity from 58% to 68% (increase of 10%) compared to clinical diagnosis. Both these studies appeared to include small difficult-to-diagnose lesions, suggesting that dermatoscopy may be most useful in these circumstances. In contrast, when clinical diagnosis was very accurate (as found by Soyer et al.15) dermatoscopy was of no benefit. This study also provided data on the accuracy of individual dermatoscopy criteria (not shown). The study by Binder et al. also examined two further important issues. They found that, although dermatoscopy had higher sensitivity than clinical diagnosis when performed by experts, it had lower sensitivity when performed by dermatologists with no formal training in the technique; these observers misdiagnosed more melanomas with dermatoscopy. Further, while experts showed moderate interobserver and intraobserver agreement (average k = 0.47 and 0.56, respectively), non-experts showed only fair agreement (average k = 0.29 and 0.36, respectively). This study used photographic slides and it may be problematic generalising these results to clinical practice. Discussion Despite the comprehensive search strategy used for this review, publication bias is still possible, and small studies of dermatoscopy with negative results may not have been submitted or accepted for publication. For dermatologists working within specialist clinics the evidence on dermatoscopy is: When sensitivity and specificity are low for clinical diagnosis of melanoma (50%-60%), both are improved by dermatoscopy performed by formally trained experts. However, when sensitivity and specificity are high for clinical diagnosis (84%-95%), dermatoscopy adds little or nothing to either. Improvement in diagnostic accuracy is most apparent for equivocal pigmented skin lesions and when using explicit structured criteria. However, as none of the studies were conducted in a primary care setting, the place of dermatoscopy in general practice is unknown. In addition, none of the studies commented that dermatoscopy improved the sensitivity and specificity of diagnosis enough to alter the clinical management of the pigmented skin lesion. In fact, dermatoscopy only increased the accuracy of diagnosis of equivocal lesions that were to undergo biopsy anyway. Given the low threshold clinicians already have for excision biopsy, the modest impact of dermatoscopy on likelihood ratios suggests it does not improve diagnostic accuracy enough to alter clinical management of most pigmented skin lesions. Further research is currently being undertaken using dermatoscopy to describe the sensitivities and specificities of individual features of pigmented lesions.6 This may prove to be more clinically relevant in the long term. In one study, the use of dermatoscopy by untrained dermatologists resulted in more melanomas being missed than with magnification alone. Non-experts also showed more interobserver and intraobserver variation. This suggests that the benefits of dermatoscopy depend on training and experience with its use. However, none of the studies commented on the type of training needed to develop competence. Two of the studies investigated the effect of using defined diagnostic criteria in diagnosing melanoma. Their results were consistent with the view that simple structured explicit criteria, such as ABCD criteria, either with or without dermatoscopy, result in a high sensitivity and specificity for diagnosis of melanoma. To provide better evidence on the value of dermatoscopy in Australian clinical practice, future research should be more explicit in the methods used and should select lesions representative of those seen in primary and secondary care in Australia. An investigation in clinical practice, where the prevalence of melanoma is low, is not practicable. However, it would be possible to compare the accuracy of diagnosis from dermatoscopic and standard magnified images of skin lesions by dermatologists and general practitioners. This type of study would also allow further assessment of intraobserver and interobserver variability and could be combined with assessment of the impact of training. This approach would allow the potential clinical benefits and limitations of dermatoscopy to be more clearly understood. Acknowledgements I gratefully thank Dr P S Morris (Menzies School of Health Research, Darwin, NT), Associate Professor L Piterman (Department of Community Medicine, Monash University, Melbourne, VIC), and three anonymous reviewers for helpful comments on an earlier draft of the manuscript; Mariella Stroschio and Antje Haase for translation of Italian and German articles; the RACGP Resource Centre librarians, Jane Ryan and Diane Horrigan, for their skills in searching Embase and hard work in locating the articles; the Royal Darwin Hospital library for use of Medline ; and the RACGP Research and Development Fund. References Kelly JW. Malignant melanomas -- how many have you missed? Med J Aust 1996; 164: 431-436. Kelly JW. Melanoma: detection and management. Aust Fam Phys 1994; 23: 801-812. Del Mar CB. How many melanomas have I missed? Is this the question? [letter]. Med J Aust 1996; 165: 456. Nachbar F, Stoltz W, Merckle T, et al. The ABCD rule of dermatoscopy. High prospective value in diagnosis of melanocytic lesions. J Am Acad Dermatol 1994; 30: 551-559. Kenet R, Kang S, Kenet BJ, Fitzpatrick TB. Clinical diagnosis of pigmented lesions using digital epiluminescence microscopy grading protocol. Arch Dermatol 1993; 129: 157-174. Menzies SW, Ingvar C, McCarthy WH. A sensitivity and specificity analysis of the surface microscopy features of invasive melanoma. Melanoma Res 1996; 6: 55-62. Irwig L, Toteson A, Gatsonis C, et al. Guidelines for meta-analyses evaluating diagnostic tests. Ann Intern Med 1994; 120: 667-676. Cochrane Methods Working Group on Systematic Review of Screening and Diagnostic Tests. The Cochrane methods working group on systematic review of screening and diagnostic tests: recommended method. [sighted 6 Oct 1996] < http://som.flinders.edu.au/FUSA/COCHRANE/cochrane/sadt.doc.html > > Nilles M, Boedeker RH, Schill WB. Surface microscopy of naevi and melanomas -- clues to melanoma. Br J Dermatol 1994; 130: 349-355. Carli P, De Georgi V, Donati E, et al. La microscopia a epilumescenza (ELM) riduce il rischio di asportare lesioni melanocitarie clinicamente sospette ma istologicamente comuni. Giornale Italiano Dermatologia e Venereologia 1994; 129: 599-605. Sackett DL, Haynes RB, Guyatt GH, et al. Clinical epidemiology: a basic science of clinical medicine. 2nd ed. Boston, Mass: Little, Brown and Company, 1991: 151-152. Steiner A, Pehamberger H, Wolff K. In vivo epiluminescence microscopy of pigmented skin lesions. 2. Diagnosis of small pigmented skin lesions and early detection of malignant melanoma. J Am Acad Dermat 1987; 17: 584-591. Cristofolini N, Zumiani G, Bauer P, et al. Dermatoscopy: usefulness in the differential diagnosis of cutaneous pigmentary lesions. Melanoma Res 1994; 4: 391-394. Binder N, Schwarz N, Winkler A, et al. Epiluminescence microscopy. A useful tool for the diagnosis of pigmented lesions for formally trained dermatologists. Arch Dermatol 1995; 131: 286-291. Soyer HP, Smolle J, Leitinger G, Kerl H. Diagnostic reliability of dermoscopic criteria for detecting malignant melanomas. Dermatology 1995; 190: 25-30. Pazzini C, Pozzi M, Betti R, et al. Improvement of diagnostic accuracy in the clinical diagnosis of pigmented skin lesions by epiluminescence microscopy. Skin Cancer 1996; 11: 159-161. Pehamberger H, Steiner A, Wolff K. In vivo epiluminescence microscopy of skin lesions. 1. Pattern analysis of pigmented skin lesions. J Am Acad Dermat 1987; 17: 571-583. McGovern TW, Litaker MS. Clinical predictors of malignant pigmented lesions. J Dermatol Surg Oncol 1992; 18: 22-26. Stoltz W, Holzel D, Riemann A, et al. Multivariate analysis of criteria given by dernatoscopy for the recognition of melanocytic lesions [abstract]. Abstracts of the Fiftieth Meeting of the American Academy of Dermatology; 1991; Dallas (TX). American Academy of Dermatology, 1991. Bahmer FA, Fritsch P, Kreusch J, et al. Terminology in surface microscopy. J Am Acad Dermat 1990; 23: 1159-1162. Stoltz W, Riemann A, Armand B, et al. ABCD rule of dermatoscopy: a new practical method for early recognition of malignant melanoma. Eur J Dermatol 1994; 4: 521-527. Lightstone A, Kopf A, Garfinkel L. Diagnostic accuracy -- a new approach to its evaluation: results in basal epitheliomas. Arch Dermatol 1965; 91: 497-501. Jaescheke R, Guyatt GH, Sackett DL. Users guide to the medical literature. 3. How to use an article about a diagnostic test: B. What are the results and will they help me in caring for my patients? JAMA 1994; 271: 703-707. Krieger N, Hiatt RA, Sagebiel RW, et al. Inter-observer variability among pathologists' evaluation of malignant melanoma: effects upon an analytic study. J Clin Epidemiol 1994; 47: 897-902. de Wit PEJ, van't Hof-Grootenboer B, Ruiter DJ. Validity of the histopathological criteria used for diagnosing dysplastic naevi. Eur J Cancer 1993; 29a: 831-839. (Received 14 Nov 1996, accepted 16 May 1997) Authors' details Danila Dilba Medical Service, Darwin, NT. Justine Mayer, FRACGP, General Practitioner; Master of Family Medicine Student (Monash University, Melbourne, VIC). Reprints will not be available from the author. Correspondence: Dr Justine Mayer, PO Box 538, Nightcliff, NT 0814. E-mail: jmayer@racgp.org.au ©MJA 1997 <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia.

Justine Mayer