Acute otitis media in children

Saturday 9 August 1997

BMJ Acute otitis media in children Fewer children should be treated with antibiotics

See p 350

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ost general practitioners in Britain would treat a child with acute otitis media with antibiotics.1 However, papers published recently in the BMJ cast doubt on the effectiveness of this policy.2 3 The authors concluded that antibiotics offer only limited benefits and that most children with acute otitis media can be managed without them. If justified, the authors’ conclusions would have important implications for British general practice. Acute otitis media is one of the commonest childhood problems seen by general practitioners. Every year, about 10% of under 5 year olds and 3.5% of 5-15 year olds are seen by their general practitioner at least once with the condition. Hence, a typical general practitioner will see about 20 children with acute otitis media every year.4 As there are more than 30 000 general practitioners in Britain, a more restricted role for antibiotics in the management of acute otitis media would lead to a substantial reduction in the prescribing of antibiotics. This in turn would result in fewer children experiencing the side effects of antibiotics and less likelihood of antibiotic resistance developing. The potential benefits of reduced antibiotic prescribing are clear, but are the authors of the two papers right to call for a more restricted role for antibiotics in the management of acute otitis media? Del Mar and colleagues carried out a meta-analysis of six randomised controlled trials.2 They found no difference in the percentage of children who still had pain 24 hours after starting treatment (39% in the treatment group v 40% in the control group). However, after two to seven days, fewer children in the antibiotic group had pain than children in the placebo group (9.7% v 14.3%). Moreover, the risk of contralateral otitis media was also reduced by 43%. There was no significant difference in the prevalence of deafness at one month or in the percentage of children with recurrent acute otitis media. Del Mar et al concluded that the early use of antibiotics provides only modest benefits, with 17 children requiring treatment at first presentation to prevent one child experiencing pain at two to seven days. However, their meta-analysis had only limited power to show whether antibiotics had an effect on some important outcomes. Thus, some differences which may be clinically significant did not achieve statistical significance—for example, a 50% reduction in the risk of perforation of the ear drum and a 20% reduction in deafness at three months in those treated with antibiotics. Furthermore, all of the trials in the meta-analysis were too small to look at rare complications like mastoiditis and meningitis. 9 AUGUST 1997

In their review, Froom and colleagues found that there are still many unanswered questions about the role of antibiotics in the management of acute otitis media.3 The benefits of antibiotic treatment on short term and long term outcomes remain unproved; uncertainty exists over whether antibiotics prevent rare complications; and it is not known whether treatment of high risk groups with antibiotics prevents poor outcomes. Furthermore, the treatment of acute otitis media varies worldwide, with a much higher use of antibiotics in the United States and in Britain than in the Netherlands.5 Despite the lower rate of use of antibiotics by Dutch general practitioners, the incidence of complications from acute otitis media is no higher in the Netherlands than in countries where antibiotics are used more frequently.1 5 Further support for a restricted role for antibiotics in upper respiratory tract infections is provided by a recent randomised trial of prescribing strategies carried out by Little and colleagues. This showed that antibiotics had little effect on the duration of symptoms in patients with sore throats.6 The authors also found, as reported in this week’s BMJ (p 350), that prescribing antibiotics for patients with sore throats had no effect on the rate of early return for medical advice or on relapse and complication rates.7 Furthermore, patients who were prescribed antibiotics were nearly 40% more likely to attend the surgery when they had another episode of sore throat. Hence, by prescribing antibiotics for mild and moderate upper respiratory tract infections, general practitioners run the risk of medicalising minor self limiting illnesses and increasing their future workload. General practitioners will need to consider all these points when determining their policy on the use of antibiotics in children with acute otitis media. They will also need to consider the opinions of clinicians who support the use of antibiotics such as Klein8 and Berman.9 Although Klein and Berman accept that only around one third of children with acute otitis media require antibiotics to help cure the condition, they advocate using antibiotics for all episodes of acute otitis media as there are currently no clinical criteria for identifying which children will need antibiotics. Further research on the management of acute otitis media is clearly needed to resolve some of the unanswered questions and to allow general practitioners to base their treatment decisions on sound evidence.2 3 10 Randomised trials should include patient and carer centred outcomes such as the absence of 321

Editorials children from school or nursery and the time parents have to take off work to look after a sick child. Any future trials should also be large enough to show how effective antibiotics are in reducing important complications of acute otitis media such as persistent deafness. Trials are also needed of the effectiveness of antibiotics in subgroups of children at high risk of poor outcomes. Until better evidence is available, most general practitioners are likely to continue to treat children with acute otitis media with antibiotics. However, where the diagnosis is in doubt or where the child is not unduly ill, a restricted use of antibiotics and a more open discussion with parents about the options for treatment would be appropriate. Azeem Majeed Senior lecturer in general practice Tess Harris Lecturer in general practice Division of General Practice and Primary Care, St George’s Hospital Medical School, London SW17 0RE [email protected]

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Froom J, Culpepper L, Grob P, Bartelds A, Bowers P, Bridge-Webb C, et al. Diagnosis and antibiotic treatment of acute otitis media: report from International Primary Care Network. BMJ 1990;300:582-6. 2 Del Mar CB, Glasziou PP, Hayem M. Are antibiotics indicated as initial treatment for acute otitis media? BMJ 1997;314:1526-9. 3 Froom J, Culpepper L, de Melker RA, Jacobs M, van Buchem L, Green LA, et al. Antimicrobials for acute otitis media? A review from the International Primary Care Network. BMJ 1997;315:98-102. 4 McCormick A, Fleming D, Charlton J, Royal College of General Practitioners, Office of Population Censuses and Surveys, Department of Health. Morbidity statistics from general practice. Fourth national study, 19911992. London: HMSO, 1995. 5 Van Buchem FL, Peeters MF, van’t Hof MA. Acute otitis media: a new treatment strategy. BMJ 1985; 290: 1033-7. 6 Little P, Williamson I, Warner G, Gould C, Gantley M, Kinmouth AL. Open randomised trial of prescribing strategies in managing sore throat. BMJ 1997;314:722-7. 7 Little P, Williamson I, Warner G, Gould C, Gantley M, Kinmouth AL. Reattendance and complications in a randomised trial of prescribing for sore throat: the medicalising effect of prescribing antibiotics. BMJ 1997;315:350-2. 8 Klein JO. Otitis media. Clin Infect Dis 1994;19:823-33. 9 Berman S. Otitis media in children. N Engl J Med 1995;332:1560-5. 10 Claessen JQPJ, Appelman CLM, Touw-Otten FWMM, de Melker RA, Hordijk GJ. A review of clinical trials regarding treatment of acute otitis media. Clin Otolaryngol 1992;17:251-7.

Kawasaki disease Early recognition is vital to prevent cardiac complications

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r Tomisaku Kawasaki described the disease that bears his name nearly 30 years ago.1 Kawasaki disease is now the commonest cause of acquired heart disease in children in developed countries. Its cause remains unknown, and it presents doctors with many difficulties in diagnosis and management. Kawasaki disease is a systemic febrile vasculitis predominantly affecting children aged under

Diagnostic criteria for Kawasaki disease Presence of at least five of six conditions: • Fever for five days or more • Bilateral (non-purulent) conjunctivitis • Polymorphous rash • Changes in lips and mouth: Reddened, dry, or cracked lips Strawberry tongue Diffuse redness of oral or pharyngeal mucosa • Changes in extremities: Reddening of palms or soles Indurative oedema of hands or feet Desquamation of skin of hands, feet, and groin (in convalescence) • Cervical lymphadenopathy: More than 15 mm in diameter, usually unilateral, single, non-purulent, and painful Exclusion of diseases with similar presentation: • Staphylococcal infection (such as scalded skin syndrome, toxic shock syndrome) • Streptococcal infection (such as scarlet fever, toxic shock-like syndrome). Throat carriage of group A streptococcus does not exclude the possibility of Kawasaki disease • Measles and other viral exanthems • Leptospirosis • Rickettsial disease • Stevens-Johnson syndrome • Drug reaction • Juvenile rheumatoid arthritis

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5 years. The incidence in Britain is 3.4 per 100 000 children aged under 5 years2—about a third of the incidence reported in the United States and a 30th of that in Japan.3 The most important complication, coronary arteritis leading to formation of aneurysms, occurs in 20-30% of untreated patients.3 Thrombosis within an aneurysm, myocardial infarction, and dysrhythmias may occur in the acute phase of the illness. The case fatality rate in Britain in 1990 was 3.7%,2 which compares unfavourably with the United States and Japan, where in some centres it is as low as 0.1%.2 Patients also suffer long term morbidity as a result of scarring of coronary arteries, intimal thickening, and accelerated atherosclerosis.3 There is no diagnostic test for the disease, and many cases are missed. Six deaths were recorded in Britain in 1990, but only one case was diagnosed during life.2 The diagnosis is based on fulfilling clinical criteria (see box).4 However, many common childhood infections have similar clinical features. Furthermore, the diagnostic features of Kawasaki disease may appear sequentially rather than simultaneously. The two features that doctors most often remember are desquamation of the rash and thrombocytosis. Unfortunately, these features are the least useful in reaching an early diagnosis because they usually occur later in the disease. Moreover, the clinical diagnostic criteria do not identify every case; “incomplete” or “atypical” cases have come to light because coronary artery aneurysms have been found on echocardiography or at necropsy.5 How can a doctor distinguish Kawasaki disease from more common causes of fever with a rash? Remaining alert to the possibility of the diagnosis is critical. Many “textbook” cases of the disease are missed simply because the diagnosis is not considered. Kawasaki disease can be mistaken for measles, but measles has become less common in Britain since the recent vaccination campaign. Kawasaki disease is a BMJ VOLUME 315

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Editorials Table 1 Treatment of Kawasaki disease Drug

Dose

Notes

Intravenous immunoglobulin

Single high dose infusion of 2 g/kg over 10 hours (reduce infusion rate in older children because of risk of fluid overload)

Reactions (shivering, fever, hypotension) are uncommon and usually managed by stopping infusion and restarting at reduced infusion rate Treatment with chlorpheniramine and hydrocortisone is occasionally required

Aspirin

30 mg/kg/day in three or four divided doses

Continue for 14 days or until fever subsides, then change to low antiplatelet dose

Acute phase of disease

Convalescent phase of disease Aspirin

3-5 mg/kg/day (antiplatelet dose) in single daily dose

If no coronary artery lesions detected on initial echocardiogram then continue until repeat echocardiogram at 6-8 weeks If coronary artery lesions are detected at any stage then continue long term

systemic disease and typically affects many systems; doctors should not be diverted from the diagnosis because of less characteristic features such as rhinorrhoea, cough, abdominal pain, vomiting, diarrhoea, pain and swelling of joints, involvement of the central nervous system, abnormal liver function tests, and sterile pyuria, which can all occur in Kawasaki disease. There are some useful clues to the diagnosis. Most of the diseases for which Kawasaki disease is mistaken do not cause fever for more than five days. In addition, the fever in Kawasaki disease is often unresponsive to antipyretics, and the child is inconsolably miserable (fig 1). An additional sign sometimes seen in the acute phase is redness and induration at the site of a BCG scar. Kawasaki disease is an inflammatory process, and an acute phase response is characteristic—its absence suggests an alternative diagnosis. Presumptive treatment should be started in any child with a persistent fever, some of the clinical features of Kawasaki disease, and an acute phase response even if symptoms do not meet the full diagnostic criteria. Intravenous immunoglobulin is the most effective treatment (see table 1). Given within 10 days of onset, this significantly decreases both the incidence and severity of aneurysm formation,6 7 as well as providing dramatic resolution of inflammation and relief of symptoms. A single high dose of 2 g/kg is more effective than the previously recommended regimen of

400 mg/kg for four days.7 However, despite its proved efficacy, many patients receive delayed or inadequate amounts of immunoglobulin, or even none at all.8 In Britain in 1990 only 7% of patients were given the recommended optimal treatment, and 39% were not given any immunoglobulin at all.3 There is often uncertainty about the use of immunoglobulin in patients diagnosed more than 10 days after the start of the disease. This has not been tested in a prospective controlled trial. However, many paediatricians recommend the use of immunoglobulin in such patients if there is evidence of ongoing inflammation, as suggested by continuing fever, malaise, and raised acute phase reactants. Retreatment with immunoglobulin is recommended for persistent or recrudescent disease. Aspirin remains an integral part of treatment, although its use in Kawasaki disease has not been subjected to prospective controlled trials.9 Many of the difficulties in diagnosing and managing patients with Kawasaki disease would be solved if the cause of the disease was known. The epidemiology strongly suggests an infectious aetiology.10 At the recent international symposium on Kawasaki disease there was much interest in the hypothesis that the disease is caused by a bacterial superantigen toxin, similar to those responsible for the staphylococcal and streptococcal toxic shock syndromes.11 The recent report of a patient who fulfilled the clinical criteria for staphylococcal toxic shock syndrome but who also had coronary artery lesions typical of Kawasaki disease12 supports the suggestion that Kawasaki disease and toxic shock syndrome share a common aetiology. However, there is still conflicting evidence for the superantigen theory. Future advances in diagnosis and treatment are likely to depend on the definitive identification of the cause of the disease. Further information: Kawasaki Support Group, Sue Davidson, 13 Norwood Grove, Potters Green, Coventry CV2 2FR. Tel (01203) 612178; http://www.sm. ic.ac.uk/paediatrics/kawa.htm.

Nigel Curtis MRC clinician scientist Paediatric Infectious Diseases Unit, Department of Paediatrics, Imperial College School of Medicine at St Mary’s, London W2 1PG ([email protected])

1

Fig 1 The child with Kawasaki disease is characteristically inconsolable (Reproduced with parents’ consent)

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Kawasaki T. Acute febrile mucocutaneous lymph node syndrome with lymphoid involvement with specific desquamation of the fingers and toes in children. Jpn J Allergy 1967;16:178-222. 2 Dhillon R, Newton L, Rudd PT, Hall SM. Management of Kawasaki disease in the British Isles. Arch Dis Child 1993;69:631-6. 3 Kato H, Akagi T, Sugimura T, Sato N, Kazue T, Hashino K, et al. Kawasaki disease. Coron Artery Dis 1995;6:194-206. 4 Dajani AS, Taubert KA, Gerber MA, Shulman ST, Ferrieri P, Freeed M, et al. Diagnosis and therapy of Kawasaki disease in children. Circulation 1993;87:1776-80. 5 Rowley AH, Gonzalez CF, Gidding SS, Duffy CE, Shulman ST. Incomplete Kawasaki disease with coronary artery involvement. J Pediatr 1987;110:409-13. 6 Furusho K, Kamiya T, Nakano H, Kiyosawa N, Shinomiya K, Hayashidera T, et al. High-dose intravenous gammaglobulin for Kawasaki disease. Lancet 1984;ii:1055-8. 7 Newburger JW, Takahashi M, Beiser AS, Burns JC, Bastian J, Chung KJ, et al. A single intravenous infusion of gamma globulin as compared with four infusions in the treatment of acute Kawasaki syndrome. N Engl J Med 1991;324:1633-9. 8 Levin M. Management of Kawasaki disease in the British Isles. Arch Dis Child 1993;69:637-8. 9 Newburger JW. Treatment of Kawasaki disease. Lancet 1996;347:1128. 10 Levin M, Tizard EJ, Dillon MJ. Kawasaki disease: recent advances. Arch Dis Child 1991;66:1369-72. 11 Curtis N, Levin M. Superantigen toxin diseases. Adv Paediatr 1996;12: 31-51. 12 Davies HD, Kirk V, Jadavji T, Kotzin BL. Simultaneous presentation of Kawasaki disease and toxic shock syndrome in an adolescent male. Pediatr Infect Dis J 1996;15:1136-8.

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Editorials

Clinical guidelines An ambitious national strategy

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he NHS Executive has published its approach to the development, appraisal, and application of clinical guidelines.1 In principle, guidelines are attractive because of the potential of standardising clinical practice around an appropriate norm. Concerns about them include the amount of time and effort required to produce and update really good guidelines, the variable quality of existing guidelines, and the danger of inadvertently suppressing innovative or patient centred care by imposing an imperfect external standard.2 3 Many of these concerns have been addressed by the NHS Executive in its document, which conveys throughout a non-directive, “light touch” approach to the effectiveness initiative. Clinical guidelines are defined as “systematically developed statements which assist clinicians and patients in making decisions about appropriate treatment for specific conditions,” a definition which is likely to be widely accepted. The authors advise against using the term “protocol” and reinforce the distinction between nationally and locally developed clinical guidelines. The status of guidelines as guidance, rather than instructions or commands, is reinforced. They are seen as aids to, not substitutes for, clinical judgment. Although anyone can, in theory, develop guidelines, the NHS Executive believes that the task of developing national guidelines is specifically the responsibility of the professional royal colleges. This approach might be considered an optimistic one since it remains to be seen whether the colleges have the resources to produce an adequate series of guidelines that consider the views of non-members—including patients and other disciplines. There are many obstacles, both practical and political, to the development of truly multidisciplinary, patient focused guidelines. The NHS Executive intends to commend for use only those guidelines that complement other centrally commissioned work, focusing their energy and resources on a few key initiatives. The Clinical Outcomes Group, a multidisciplinary group set up by the executive, will be responsible for endorsing suitable guidelines that the executive can then safely promote for use in the NHS. The outcomes group will classify guidelines according to the quality of evidence on which they are based. Only those based on randomised controlled trials will be recommended for use in contracts. The danger is that areas which are not a current priority, and therefore already relatively neglected in terms of funding and research attention, will be further disadvantaged because guidelines relevant to them will not be endorsed. The insistence on evidence from randomised controlled trials, although in many ways commendable, could cause further bias. Some clinical areas—for example, rehabilitation and learning disability—do not lend themselves easily to this research design.4 5 Responsibilities are clearly set out for the professional royal colleges (development of guidelines), the Clinical Outcomes Group (endorsement), and the NHS Executive (commending endorsed 324

guidelines to the service), but certain other responsibilities remain vague. For example, it is not clear who will appraise guidelines (on behalf of the Clinical Outcomes Group) independently of the professions and the NHS Executive, or who will be responsible for ensuring that guidelines are implemented locally across all relevant disciplines. The potential conflict between local and national guidelines is not explored, yet this may be one of the most difficult problems. There is a paradox in that local ownership is often held to be related to use while national guidelines are seen to be more firmly based on empirical research. In fact, the evidence that national guidelines are more difficult to implement is not robust.6 Further research on the mechanisms governing the implementation of guidelines is required to clarify this whole area. With the possible exception of the Clinical Outcomes Group, no new organisations have been set up, or are planned, to push guidelines into practice. This approach relies heavily on traditional responsibilities and differs greatly from that adopted in the United States and in Scotland, where the development, implementation, and monitoring of guidelines is overseen by custom built organisations. Monitoring is also a weak area of the strategy. The Clinical Standards Advisory Group has a role in this, and has already studied the use of guidelines in elective surgery7 and strokes, but it investigates only about two clinical areas each year. At least one of the national research and development programmes lists guideline evaluation as one of its top priorities. Surely this objective should be generalised to other areas? The NHS Executive is committed to the development and adoption of high quality national guidelines as the most tangible means of improving the clinical effectiveness of care in the NHS. This could be seen as a move away from supporting an alternative approach to the same problem—namely, local clinical audit. However, guidelines and recommended pathways of care can provide the ideal structure for effective audit. The executive’s plan is likely to be broadly supported but needs a clear plan for evaluation to ensure that guidelines do after all promote clinical effectiveness across the full spectrum of professional practice. Elizabeth West Research sociologist John Newton Consultant epidemiologist Unit of Healthcare Epidemiology, Institute of Health Sciences, University of Oxford, Oxford OX3 7LF

1 2 3 4 5 6 7

Mann T. Clinical guidelines: using clinical guidelines to improve patient care within the NH. Leeds: NHS Executive, 1996. Hopkins A. Some reservations about clinical guidelines. Arch Dis Child 1995;72:70-5. McKee M, Clarke A. Guidelines, enthusiasms, uncertainty, and the limit to purchasing. BMJ 1995;310:101-4. Newton J, West E. Evidence-based medicine and compassion. Lancet 1996;347:1839. Black N. Why we need observational studies to evaluate the effectiveness of health care. BMJ 1996;312:1215-8. NHS Centre for Reviews and Dissemination. Implementing clinical practice guidelines. Effective Health Care Bulletin 1994;8. Newton J, Metcalf MC. District elective surgery. London: Clinical Standards Advisory Group, 1996.

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Editorials

Why Britain’s drug czar mustn’t wage war on drugs Aim for pragmatism, not dogma

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he British government has advertised the first ever post of drug supremo, or ‘drug czar’ to borrow the term used in the United States. It is good news that the new Labour government is evidently serious about the growing national and international drug problem and intends to strengthen further the pan-departmental approach taken by the central drugs co-ordinating unit and its strategic document for England, Tackling Drugs Together.1 But there is a grave danger that the increased political attention could backfire, producing a more politicised approach to the problem and causing the new czar’s dominant orientation to be one of control. Crime dominated posturing would lead to a damaging dissociation between the public appeal of the policy and actual evidence of effectiveness. It could lead to a mistaken bias to funding more panda cars, prisons, and pop propaganda instead of evidence-based treatment, rehabilitation, and preventive strategies. In contrast, diverting limited resources from enforcement to treatment and rehabilitation would result in more cost-effective crime prevention and community safety. Prisons are already bursting with new inmates on remand or sentence for addiction fuelled crime; it would be criminal negligence to spend yet more on control whilst demand for treatment still far outstrips capacity. The ‘war’ rhetoric is particularly dangerous. It is therefore disappointing that the new post draws its ‘czar’ title from the United States—a strange role model to select considering its vastly greater prevalence of drug misuse2 —and is charged with leading the ‘battle against drugs.’ The macho nature of the post is further signalled by its title—no czarina need apply. If this imagery is not to misfire, the new supremo must understand UK drug policy. In the UK, pragma has trumped dogma. This has allowed, for example, anti-HIV approaches such as needle and syringe exchange3 nearly a decade earlier than the US, thus preventing the apparently inevitable epidemic of HIV infection among drug injectors.4 Other examples of pragmatism include the tolerance of at least some prescribing of injectable heroin and methadone.5 Britain should be proud of its capacity to put rhetoric aside and pursue strategies which best benefit the health of the nation. The nature of the war on drugs needs to be understood. War it is, but not in the sense conveyed by the government’s job advertisement. For it is a war that will never be won, and yet against which we must continue to battle, just as with the war on cancer and the war on poverty. In this war, it is public health physicians and town planners who should be our generals; and doctors, drug workers, and community policemen should be our foot soldiers. As we have previously argued,6 for each of these unwinnable wars it is imperative to direct our available resources to fight on the right fronts—those on which we have good reason to believe that advances will be made as a result of our activities. The new czar will need to follow the lead of evidence based medicine: redirecting funds into those treatments BMJ VOLUME 315

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with demonstrable effectiveness, which may not be the same as the most popular; applying an evidence based strategy to areas such as drug control and education; and altering the balance of funding—between control, treatment, and education—on the basis of these findings. A stronger treatment arm to the drug strategy is vital. The previous UK drug strategy in 19951 represented a clear swing to a crime dominated perspective and was in sharp contrast to the dominant public health perspective on AIDS and drug misuse in the late 1980s.7 However, the picture is now different. Not only is the new government intent on being tough on the causes of the drug problem as well as tough on the problem itself, but we also now have good evidence of multiple benefits from some treatments. For example, we have international evidence of reduced levels of drug use, injecting, and criminal behaviour with methadone maintenance in patients addicted to opiates.8 9 Three messages should be pinned above the new czar’s desk. Firstly, be clear about the objectives of a new drug strategy, with the reduction of damage to individuals and society as the guiding principle. Secondly, look beyond the many examples of failing drug strategies to the growing evidence base for alcohol and tobacco policies:10 11 this would allow the drug strategy to be developed appropriately alongside emerging strategies for alcohol and smoking. And finally, be determined in pursuit of evidence based strategy, incorporating elements not for political or professional popularity but according to the quality of evidence of benefit to individuals and the public. If the evidence does not currently exist, the czar should set aside perhaps 1% of the budget to establish centres charged with correcting the poverty of research output in this field in Britain.12 Science would then properly serve the policy making process, and the appointment of a UK drug czar would be a true step forward. John Strang Director National Addiction Centre, 4 Windsor Walk, London SE5 8AF

William B Clee Chair Welsh Advisory Committee on Drug and Alcohol Misuse, Parc-Caonl Practice, Church Village, Rhondda-Cynon-Taff, South Wales

Lawrence Gruer Consultant in public health medicine HIV and Addictions Resource Centre, Ruchill Hospital, Glasgow G20 9NE

Duncan Raistrick Director Leeds Addiction Unit, 19 Springfield Mount, Leeds LS2 9NG

1 2

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HM Government. Tackling drugs together: a strategy for England, 1995-1998. London: HMSO, 1995. Kleber H. The US anti-drug prevention strategy: science and policy connections. In: Edwards G, Strang J, Jaffe JH, (Eds). Drugs, alcohol and tobacco: making the science and policy connections. Oxford: Oxford University Press, 1993:109-20. Stimson GV, Alldritt L, Dolan K, Donoghoe M, Lart R. Syringe exchange schemes for drug users in England and Scotland. BMJ 1988;296:1717-9. Stimson GV. AIDS and injecting drug use in the United Kingdom, 19871993: the policy response and prevention of the epidemic. Soc Sci Med 1995;41:699-716. Strang J, Ruben S, Farrell M, Gossop M. Prescribing heroin and other injectable drugs. In: Strang J, Gossop M, eds. Heroin addiction and drug policy: the British system. Oxford: Oxford University Press, 1994:192-206.

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Strang J. Injecting drug misuse: response to Health of the Nation. BMJ 1991;303:1043-6. Advisory Council on the Misuse of Drugs. AIDS and drug misuse: update report. London: HMSO, 1993. Ball JC, Ross A. The effectiveness of methadone maintenance treatment: patients, programs, services and outcome. New York: Springer, 1991. Farrell M, Ward J, Des Jarlais DC, Gossop M, Stimson GV, Hall W, et al. Methadone maintenance programmes: review of new data with special reference to impact on HIV transmission. BMJ 1994; 309:991-1001.

10 Edwards G, Anderson P, Babor T, Casswell S, Ferrence R, Giesbrecht N, et al. Alcohol policy and the public good. Oxford: Oxford University Press, 1994. 11 Raw M, McNeill A. The prevention of tobacco-related disease. Addiction 1994;89:1505-9. 12 Department of Health Task Force. The Task Force to review services for drugs misusers: report of an independent survey of drug treatment services in England. London: Department of Health, 1996.

Educating doctors, to improve patient care A choice between self directed learning and sitting in lectures struggling to stay awake

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he postgraduate education allowance for general practitioners in the UK was introduced in 1990, amidst the turmoil of the “contract row” between the secretary of state for health and general practitioners. It makes up just under 5% of general practitioner’ intended net remuneration, replacing direct reimbursement of educational expenses under “section 63” with a payment to which conditions are attached. To qualify for the allowance, general practitioners must satisfy regulations of byzantine complexity, the essence of which is the requirement to attend 30 hours of approved continuing education in each of the previous five years. Educational theory, supported by research and most people’s experience, suggests that active learning—in small groups, using interactive computer packages, or even reading—is more likely to change clinical behaviour than sitting in large lecture theatres struggling to stay awake. But for many general practitioners, the allowance poses bureaucratic hoops through which they jump with the minimum possible effort and cost. Lectures, ideally free and therefore sponsored by drug companies, are the easiest way to do this. A paper in this week’s BMJ suggests that more and more general practitioners take this route (p 353).1 The authors suggest that educational expenses should be directly reimbursed. The London initiative zone educational incentives programme (LIZEI), which was intended to help develop primary care and improve morale among general practitioners, provides valuable experience of this direct approach. Since 1995, general practitioners in the London initiative zone who produce a personal development plan can obtain funding for educational costs and protected time. They have to make clear what impact their plan will have on patient care and how they will measure this. It is too early to tell whether the London initiative zone educational incentives programme will improve patient care; but even asking doctors to think about the impact they expect their education to have on patients is a step forward. It is not, however, cheap. Considerable educational support is needed to develop and implement an effective education plan, and it often encourages the more expensive forms of education such as Master’s degrees, diplomas, or the membership exam for the Royal College of General Practitioners. The government has recognised that the postgraduate education allowance is unsatisfactory, and the chief medical officer is currently conducting a 326

review. Devising a satisfactory new system will not be easy. Direct reimbursement of expenses is not without problems. Section 63 covered course fees, travel, and subsistence, and general practitioners could choose which if any courses to attend and where to study. Some obtained great educational benefit at reasonable cost, some took no public part in continuing education, whilst others travelled to distant parts of the UK at public expense for their courses. There was no attempt to link the costs to benefit to the NHS. The postgraduate education allowance has at least ensured almost universal participation, and has largely avoided accusations of sleaze which would no doubt be rampant if the system had continued unchanged. The purpose of continuing medical education is the improvement of services to patients. The refreshment of professional enthusiasm that comes from interacting with colleagues and encountering new ideas is only a means to that end, albeit worthwhile in itself. Section 63 and the postgraduate education allowance both emphasise process rather than outcome, largely because it is easier to measure. There are no free lunches, and if the NHS pays for general practitioners’ continuing education then it has a right to expect evidence that this is likely to improve patient care. However, professional leadership and freedom of choice are essential if education is to generate the enthusiasm needed for it to be effective. Striking the right balance will not be easy. The allowance’s arbitary classification of educational activity, and the incomprehensible concept of a “course” of study, stem from the scheme having been introduced unpiloted and without sufficient forethought. The London initiative zone educational incentives programme too has faced problems resulting from lack of advanced planning and preparation. There must be time for any new system to be thoroughly planned, and for those who have to make it work to understand its philosophy and its mechanisms. Only thus will we avoid jumping out of the frying pan into the fire, and have a continuing professional development system to deliver “a service with ambition.”2

See p 353

Peter Toon General practitioner 206 Queensbridge Road, London E8 3NB ([email protected])

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Murray TS, Campbell LM. Finance, not learning needs, makes general practitioners attend courses: a database survey. BMJ 1997;315:353. Secretary of State for Health. The National Health Service. A Service with Ambition. London: HMSO, 1996.

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