Otitis media with effusion in children Surgery for otitis media with effusion (glue ear) is the carried out in childhood in industrialised countries.1 Otolaryngologists operate for one or more of three reasons: to restore the level of hearing; to prevent complications such as cholesteatoma; and to avoid developmental and behavioural problems. Research on the effectiveness of surgery has concentrated on the first of these items. Randomised controlled trials suggest that clinically significant short-term improvements in hearing can be achieved in the severest cases.2,3 However, because of difficulties in case definition, many children undergoing surgery do not benefit substantially. Otolaryngologists justify operating in children with milder hearing impairment on the grounds that surgery will prevent both complications and developmental delay. Until now there has been no convincing evidence to support these claims, but publication of a large longitudinal study from New Zealand sheds some light on the issue.4 In the Dunedin Multidisciplinary Health and Development Study, a cohort of over 1000 children born between April, 1972, and March, 1973, have been followed regularly. Every two years from the age of five, the children have undergone otological examinations, pure tone audiometry, and impedence audiometry, and developmental and behavioural tests have been conducted every two years from the age of three. The data have been studied by means of a series of cross-sectional analyses and a longitudinal analysis. After the condition of the middle-ear had been determined by impedance audiometry, cross-sectional analyses showed that the only children whose scores on developmental and behavioural tests differed significantly from those of healthy children (bilateral type A tympanograms) either had bilateral flat tympanograms (type B) or had had tympanostomy tubes (grommets) inserted. This "diseased" group displayed poorer verbal comprehension and expression at three and five years of age, and a lower intelligence quotient and poorer classroom behaviour at five years. There were no differences in the children’s articulation skills or in parental reports of behaviour problems. By the age of seven, tests did not show any significant differences in development or behaviour between children who had had audiometric evidence of otitis media at younger ages and those who had not. The longitudinal analysis concentrated on the most severely affected children-those who at the age of five had type B tympanograms plus evidence of middle ear effusion on otomicroscopy. The adverse effects on development and behaviour found in the cross-sectional analyses were confirmed. Furthermore, in the longitudinal study, poor articulation and expression together with poor reading ability and classroom behaviour were still evident at the age of nine. commonest


What are the policy implications of these findings? The Dunedin researchers suggest that there is an urgent need for the detection and management of early onset otitis media. This exercise would require the introduction of screening programmes to identify cases and almost certainly necessitate expansion of existing otolaryngology services to meet the additional demand of surgery. Before embarking on such a course a few questions need to be answered. How convincing is the evidence that early onset otitis media causes developmental and behavioural disorders? Whilst the longitudinal data are fairly the consistent-with exception of verbal is which unaffected after the age of comprehension, five-the same cannot be said about the crosssectional analyses. There is no "dose-response" relation in terms of either duration of otitis media or severity of the condition. To what extent are the statistically significant differences in development socially important? Would such differences substantially jeopardise the educational potential of these children? For how long would such effects last and would the children catch up later? If one accepts for the moment the conclusion of the Dunedin workers that 4-5% of five-year-olds have severe otitis media and suffer developmentally as a result, what can be done to help them? There is evidence that the hearing levels of such children can be improved in the short term by myringotomy and insertion of tympanostomy tubes but no evidence of a beneficial effect on development and behaviour. There is an urgent need for a randomised controlled trial in this area; any such study must ensure that the adverse as well as the beneficial effects of surgery are included. As the Dunedin study shows, tympanostomy tubes are not trouble-free-a purulent discharge or granulation tissue developed in 11 % of ears, surgical repair of tympanic membrane perforations was required in 3%, retraction pockets developed in 4%, and atrophic scars or tympanosclerosis developed in 61%. Meanwhile, there was no evidence of any serious complications of the disease itself. Thus the claim that untreated otitis media may lead to conditions such as cholesteatoma remains unsubstantiated. That surgery has potentially harmful effects is not justification for withholding treatment; rather it is a reason to ensure that only those children who can benefit are treated. Whilst there was already sufficient evidence to justify operation in the severest cases to restore hearing, the Dunedin study has shown the harm that such hearing deficiencies can have on a child’s development. Whether this new evidence will widen the appropriate indications for surgery is unclear. It may be that the children with the poorest hearing are also those who have the most

developmental delay. Otolaryngologists should that general concern for a child’s development



is not used as an excuse to further inflate the high rate of surgical interventions. 1. Black N. Surgery for glue ear-a modem epidemic. Lancet 1984; i: 835-37. 2. Maw AR, Herod F. Otoscopic, impedance, and audiometric findings in glue ear treated by adenoidectomy and tonsillectomy. Lancet 1986; i: 1399-402. 3. Black NA, Sanderson CFB, Freeland AP, Vessey MP. A randomised controlled trial of surgery for glue ear. Br Med J 1990; 300: 1551-56. 4. Chalmers DC, Stewart I, Silva P, Mulvena A. Otitis media with effusion in children-the Dunedin study. Clin Dev Med 1989; 108.


Eighteen months ago we gave the newly launched beta-1selective adrenoceptor partial agonist xamoterol a guarded welcome as a potentially useful additional treatment for at least some types of heart failure.! Since then further work has confirmed that xamoterol therapy gives modest improvements in haemodynamic function, symptoms, and exercise tolerance in patients with mild to moderate chronic heart failure (CHF).2-6 This week, however (see p 1), we publish a placebo-controlled trial involving patients with severe CHF in whom treatment with xamoterol was associated with an increase in mortality. This comes at a time when concern has been expressed in the British press (both lay and medical) about the use of xamoterol. Clearly the role of this agent in the treatment of heart failure needs to be reassessed in the light of the new study and other recent evidence. Two points about the present study should be reiterated. Firstly, it was not originally designed to examine the effect of xamoterol on mortality. Because of this, details of the mode of death and its temporal relation to initiation of xamoterol treatment are not well defined. Secondly, this study was conducted in a group of patients with severe CHF, most of whom have coronary artery disease. An increase in death due to pump failure soon after the introduction of xamoterol would suggest a detrimental effect of beta-blockade (xamoterol reduced daytime heart rate in these patients). Alternatively, an increase in myocardial infarction or ventricular arrhythmias would support a detrimental effect of the beta-agonist effect of xamoterol (nocturnal heart rate was increased). These possibilities have very different implications for future use of the drug. Restriction of prescribing to those with mild heart failure, in whom beta-blockade is not seen at rest, should greatly reduce the hazard of acute myocardial depression. However, it has also been suggested that mild heart failure progressses to severe heart failure and in the process the patient becomes increasingly dependent on the sympathetic nervous system for inotropic support. Consequently xamoterol, while initially exerting a beneficial positive inotropic action, could eventually exert a detrimental negative inotropic one. Whether CHF does progress in this way is not at all clear. Nor is it certain that sympathetic activation is good rather than bad. It is also possible that xamoterol could prevent deterioration (long-term beta-blockade may augment rather than diminish catecholamine responsiveness in CHF). Either way, if the original premise is held, the drug can be stopped if CHF does worsen. The second possibility, that increased mortality reflects an effect of beta agonism rather than antagonism, should also apply to patients with milder forms of CHF and is therefore a greater worry. The limited evidence does not

concern. Ambulatory electrocardiography in a of patients in the present study did not show an increase in ventricular arrhythmias, and in previous studies xamoterol has not been found to aggravate myocardial ischaemia. Furthermore, four-year follow-up data are available on 221 UK patients with mild CHF initially randomised to a three-month comparison of xamoterol and placebo (on completion, "open label" xamoterol was continued in responders). Survival, by "intention to treat" analysis, was 80% in the xamoterol group and 75% in the placebo group.s Thus, while the verdict on efficacy is good, that on safety is "not proven"; a prospective mortality study in mild CHF is needed to clear xamoterol. For the moment at least, the British Committee on Safety of Medicines has judged that the risk-benefit ratio for xamoterol, used carefully, in mild CHF is acceptable. How can xamoterol be prescribed safely? Only patients with mild heart failure should receive the drug. Post-marketing surveillance by the Drug Safety Research Unit in Southampton has shown that xamoterol, despite advice to the contrary, has frequently been prescribed to patients with severe CHF.99 Consequently it is now mandatory that patients undergo full investigative and functional evaluation (ECG, chest radiograph, echocardiogram, and exercise test). If indicated xamoterol should then be started-in hospital, under supervision. These precautions could be more widely applied. Heart failure is a complex syndrome of multiple aetiologies requiring precise diagnosis and tailored therapy. For good management of this common and disabling condition, patients need to be assessed individually; for some, the treatment may still include xamoterol.

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1. Editorial. Xamoterol: stabilising the cardiac beta receptor? Lancet 1988; ii: 1401-02. 2. The European ’Corwin’ Study Group. Xamoterol in mild to moderate

heart failure: a subgroup analysis of patients with cardiomegaly but no concomitant angina pectoris. Br J Clin Pharmacol 1989; 28 (suppl 1): 675-95. 3. Bostraom PA, Johansson BW, Lecerof H, Lilja B, Torp A. Effect of xamoterol on exercise capacity and left ventricular function in angina pectoris and in dilated cardiomyopathy. J Intern Med 1989; 226: 331-35. 4. Waller DG, Webster J, Sykes CA, Bhalla KK, Wray R. Clinical efficacy of xamoterol, a &bgr;1-adrenoceptor partial agonist, in mild to moderate heart failure. Eur Heart J 1989; 10: 1003-10. 5. Virk SJS., Anfiologoff NH, Lawson N, et al. The acute effects of intravenous xamoterol on resting and exercise haemodynamics in patients with mild to moderate heart failure. Eur Heart J 1989; 10: 227-34. 6. Vigholt-Sorensen E, Faergeman O, Snow HM. Effects of xamoterol, a &bgr;1 adrenoceptor partial agonist, in patients with ischaemic dysfunction of the left ventricle. Br Heart J 1989; 62: 335-41. 7. Heilbrunn SM, Shah P, Bristow MR, Valantine HA, Ginsburg R, Fowler MB. Increased &bgr;-receptor density and improved hemodynamic response to catecholamine stimulation during long-term metoprolol therapy in heart failure from dilated cardiomyopathy. Circulation 1989; 79: 483-90. 8. Marlow HF, Lewis JA. Effects of xamoterol on mortality in mild to moderate heart failure (abstr). Eur Heart J (in press). 9. PEM News 1990, no 6.


Anderson-Fabry disease (angiokeratoma corporis diffusum) is a pleotropic genetic disorder. Deficiency of the lysosomal enzyme a-galactosidase results in widespread tissue accumulation of uncleaved glycosphingolipids, chiefly trihexosyl ceramide. The gene for this enzyme has been mapped to the middle of the long arm of the X chromosome. As might be expected with a slowly progressive storage disorder, the clinical manifestations are

Otitis media with effusion in children.

23 Otitis media with effusion in children Surgery for otitis media with effusion (glue ear) is the carried out in childhood in industrialised countri...
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