How many times have you heard these words spring unthinkingly from a pharmacist's lips? These words usually precede an explanation; or at least something which the speaker heartily believes passes for an explanation. Let me give you an example; "What they do is give the patient high-dose oral chlorpromazine and if that hasn't worked after a week, they add in a depot."
What can one infer from the use of "what they do is....."? And what's wrong with saying it? In short, lots and a lot, respectively. When a pharmacist begins with "what they do is....", we can deduce several things. "They" usually refers to the prescriber. Pharmacists describe what prescribers do because they, the pharmacist, do not know why the prescriber does it. The pharmacist generally has little or no knowledge of the literature relating to the issue in hand and they may have little experience (clinical, practical experience, that is) of the use of the drugs in question. The pharmacist therefore relies on what actually the prescriber does as a yardstick for good practice.
Of course, such a process would be acceptable were all prescribers sufficiently knowledgeable, sensible and logical to do what is best for the patient at all times. But they are not. Indeed, if they were, for what would society need pharmacists? It follows that pharmacists who derive their knowledge wholly from the (often unsupported) actions of prescribers are being paid to do nothing. Nothing clinical, at least. And what else are pharmacists for? Managers can manage and technicians can dispense.
Some pharmacists take pride in explaining "what we do is.....". By saying this, they implicitly include themselves in therapeutic decision making. Perhaps they even apply some evidence-based medicine mixed with their own clinical experience. But explanations beginning like this are far from satisfactory; they explain nothing.
Let us all stop repeating these glib prefixes. Let us all start saying things like "this practice is not supported by well-conducted research", "this treatment protocol is evidence-based", "I strongly recommend that ....". I, the pharmacist, who has studied long and hard, gained valuable therapeutic experience, and who is a bang up-to-date expert in psychotropic drug use.
Let us no longer tell each other what "they" do but what we, as experts, think and believe. But before that, perhaps we should first make sure that we are indeed experts.
David M. Taylor, Chief Pharmacist, Bethlem and Maudsley NHS Trust and Honorary Lecturer, Institute of Psychiatry. (April 1997)
Ask any group of pharmacists involved in mental health services about areas of prescribing which concern them and a substantial number will say "anticholinergics". Pharmacists as a group perceive that too many patients receive regular anticholinergics and that getting these prescriptions stopped is their personal mission in life.
Prescribers find this irritating. Patients are unlikely to thank you either. There are many areas of psychiatry where pharmacists can use evidence from good clinical studies to improve patient care. How many of us counsel patients to continue their antidepressants for at least six months after recovery or advise against constantly restarting lithium in poorly compliant patients? Do we always manage to keep risperidone doses to below 8mg/d or prevent the widespread use of carbamazepine 100mg tds as a mood stabiliser? These issues, and many others, are more worthy of our attention than anticholinergics.
Anticholinergics can be abused, they cause dry mouth/constipation/blurred vision and, we all repeat, do not stop the development of tardive dyskinesia. But, do we stop to consider that schizophrenia leads to TD, as do neuroleptics, particularly in those with affective illness. Neuroleptics cause dystonias, pseudoparkinsonism, akathisia and dysphoria which are all unpleasant. If a patient says that procyclidine helps, how strongly should we argue? We are, after all, moving away from compliance towards concordance: a joint decision made by the prescriber and patient. It is a well established fact that patients who experience EPSEs early in treatment are more likely to develop TD. They are also, for obvious reasons, more likely to receive anticholinergics. There is little convincing evidence that anticholinergics cause TD. After all, if it was that simple, would clozapine not pose a significant risk, rather than be a potential treatment?
It would be wrong to say that anticholinergics are completely harmless, but let's turn our attention and preoccupation to matters that are more important and where our interventions really can make a difference.
Carol Paton, Principal Pharmacist for Oxleas NHS Trust, Bexley Hospital, Bexley, Kent. (July 1997)
1997 sees the launch of two new drugs for the symptomatic treatment of Alzheimer's Disease. Aricept (Pfizer) is already available and Exelon (Novartis) is likely to be available later this year.
The launch of donepezil has certainly caused a great deal of discussion and debate in my Trust. We estimate that within our catchment area, there may be as many as 2,000 patients who would benefit from treatment. However, there is a problem. There simply is no provision in our budgets for these new drugs. The availability of these drugs follows other financial shocks: the continued promotion of newer antidepressants and atypical antipsychotics, has resulted in a dramatic rise in our drug costs. We have welcomed these innovations, we recognise the advantages they have over older drugs, but both ourselves and the purchasers of our services are reeling from the impact on our drug budgets.
What is different about these drugs for the treatment of Alzheimer's Disease is that they represent a new therapeutic class and a new and exciting therapeutic option. When considering costs, we are not updating an already established treatment, we are introducing something completely new. The question is can we afford it? If we cannot afford it, do we refuse treatment, or ration it? These are serious ethical, as well as financial, dilemmas.
A comment made by a senior clinician in my Trust is that if we can find resources to fund the use of these new drugs for the treatment of Alzheimer's disease, we should spend it instead on hip replacements as there is better evidence of cost-effectiveness and long term benefits.
A Realistic Perspective
It is important that we are clear about what these new drugs do and do not offer. Centrally acting acetylcholinesterase inhibitors are not curative. They provide modest benefits in slowing the rate of cognitive decline, without affecting the neurodegenerative changes occurring as a consequence of the disease. Patients and carers can expect between six months and two years slowing of cognitive decline, which for this limited period of time will maintain a higher degree of independence and improved quality of life. Whether these drugs will increase life expectancy is as yet unknown.
Moreover, these drugs are not global anti-dementia drugs. They are useful only in the symptomatic relief of mild to moderate Alzheimer's Disease. Therefore, as far as possible, other forms of dementia should be excluded and a more extensive clinical assessment of cognitive impairment is required.
Costs of Alzheimer's Disease
The management of all forms of dementia is extremely costly. Health costs include pressure on primary care services, cost of drugs, community focused hospital services and in-patient costs. Social costs include community support services, residential and nursing home care and cost burdens on patients themselves or on relatives who may give up work to care for the patient, or contribute to the cost of residential care which is means-tested.
What the impact on costs of new drugs will be is impossible to say with any degree of certainty, but an informed opinion would suggest that drug costs will increase markedly, but the need for costly hospital admission and subsequent residential or nursing home care will be delayed. Delayed, but not prevented. There may be increases in costs of community support services, including increased involvement of CPNs. In addition, the need for more extensive clinical investigations is also likely to increase costs.
Another contributing factor is likely to be pressure from patients and carers for more pro-active treatment. Prescribers and pharmacists often treat the advent of new drugs with caution and the use of new drugs is often limited initially. But in this case, because of the limited timescale in which patients can be expected to benefit, pressure to prescribe may be irresistible. Trusts and prescribers who attempt to limit prescribing may well have to face accusations of rationing healthcare and ageism, which could have political consequences.
A Clinical Rationale
For all of these reasons, it is important to establish a clear clinical rationale for prescribing these drugs. Procedures should be put into place to ensure that only those patients who are likely to benefit will receive them. This may include more extensive use of CT scanning and use of more sensitive instruments such as ADAS (Alzheimer's Disease Assessment Scale). It may be appropriate to limit initiation of prescribing to consultant psychiatrists only, with shared care protocols for GP prescribing, with provision for regular audit.
John Donoghue, Principal Pharmacist, Psychiatric Services, Wirral Hospital Trust (July 1997)
For some time now, there has been concern about whether or not we should use antipsychotics to treat behavioural disorders in dementia. More recently this concern has been revived due to the suspicion that antipsychotics hasten cognitive decline in dementia.
Most pharmacists would agree that an agitated and distressed patient with cognitive impairment should be treated. To decide whether or not to use an antipsychotic, let us consider what we know from research and clinical experience:
Considering the above, surely antipsychotics should only be used to treat behavioural disorders in dementia if:
To date, there has been no published research showing a causal relationship between antipsychotic drug use and cognitive decline in dementia. Randomised controlled trials are unlikely to take place for ethical reasons. Taking into account what we already know about antipsychotics in dementia, does it really matter whether they hasten cognitive decline or not?
Ann Hutton, Clinical Pharmacist, Bethlem and Maudsley NHS Trust (October 1997)
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