The Editorial Executive Committee welcomes letters, which should be less than 250 words. Before a decision to publish is made, letters which refer to a published article may be sent to the author for a response. Any letter may be sent to an expert for comment. When letters are published, they are usually accompanied in the same issue by their responses or comments. The Committee screens out discourteous, inaccurate or libellous statements. The letters are sub-edited before publication. Authors are required to declare any conflicts of interest. The Committee's decision on publication is final.
Editor, – As a dentist, I am particularly concerned with guidelines for the prevention of endocarditis. The new Antibiotic Guidelines1 differ from previous editions by giving only one set of recommendations for patients with cardiac lesions, which predispose them to infective endocarditis. These include congenital or rheumatic heart disease, a previous episode of endocarditis, and the presence of prosthetic heart valves. In previous editions there were guidelines for low-risk patients (those suffering from congenital or rheumatic heart disease) and for high-risk patients (those with prosthetic heart valves or a previous episode of endocarditis).2 The prophylaxis for low-risk patients was 3 g oral amoxycillin given one hour before dental treatment. For high-risk patients this was supplemented with gentamicin 2 mg/kg.
In the new edition the dose of amoxycillin is reduced to 2 g and there is no additional drug for high-risk patients. I am unhappy about the omission of the category of high-risk patients because I am aware of three cases where oral amoxycillin failed to prevent the occurrence of endocarditis. A recent British paper3 continues to advocate a supplementary antibiotic for high-risk patients.
The editors of the Antibiotic Guidelines do not explain these changes. They state 'Consensus is currently changing and these recommendations are based upon current international practice'. It would seem that on the whole the guidelines of the American Heart Association4 were followed. Would it not be more logical to base the new recommendations on an analysis of case histories? One way of approaching this difficult subject would be by analysing instances where previous recommendations for prevention had failed. Unfortunately there is no central body responsible for listing such failures. The last such study5 was published in 1982. We can only ascertain whether the prophylactic measures suggested by various authorities are effective or not, if records are kept.
It is unfortunate that guidelines for the prevention of endocarditis differ from country to country. I agree with the suggestion that we should have uniform guidelines throughout the world.6
E.H. Ehrmann
Senior Fellow
School of Dental Science
Faculty of Medicine, Dentistry and Health Science
University of Melbourne
Melbourne
Professor W. John Spicer, Chairman, and Dr David Looke, Member, Writing Group for Antibiotic Guidelines, comment:
We empathise with Dr Ehrmann's difficulties. These difficulties stem from one currently insuperable problem in writing guidelines for endocarditis prophylaxis; there are no accurate, quantitative data on:
- the risks of particular procedures
- the risks of particular cardiac lesions
- the results of particular antibiotic regimens.
The Antibiotic Guidelines have been evidence-based for over 20 years, but in endocarditis prophylaxis, the evidence is like the Dead Sea Scrolls. It is fragmentary, imperfect, capable of various interpretations, or (mainly) missing!
Another problem in countries like Australia is that it is difficult logically or medicolegally to differ from major overseas guidelines when there are no data to show whether the outcomes of a different Australian recommendation would be similar, better or worse.
To address Dr Ehrmann's specific difficulties:
There is no good evidence to continue the practice of low-risk/high-risk stratification.
Three grams of amoxycillin was recommended originally simply because of the availability of that formulation. Pharmacokinetic data show that 2 g is enough. Certainly, 3 g is too much for some patients to tolerate. Whether or not a second dose would prevent endocarditis not prevented by a single dose, is pure conjecture.
There is no good evidence that gentamicin is necessary or effective in prophylaxis (as distinct from treatment). We have therefore moved towards the American and British recommendations.
Dr Ehrmann's comments are welcome and constructive. In this area with so little hard evidence, opinion must be gathered, weighed and synthesised into coherent recommendations. Variation is acceptable if good reasons and particular circumstances exist. Compromise is inevitable, and disagreement predictable.