White elephants about town

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EDITORIAL

White elephants about town expanding urban population in many developing countries is causing a crisis in provision of public services. Inadequate local health services for low-income groups and long queues of patients at hospitals have prompted health planners to explore the best ways of improving government health facilities. The World Health Organization, in an The

attempt to assist health ministries in this process, has recommended the setting up of "reference centres", a new tier in the health system between existing hospitals and health centres.1 The aim of these centres is to provide first-contact medical services 24 hours a day, obstetric services, diagnostic facilities, and inpatient care. Within their prescribed catchment area, a reference centre is responsible for the work of health centres, for community development, and for public health activities. Thus in effect reference centres are indistinguishable from small district hospitals, and they are expected to relieve the perceived overload at existing specialist city hospitals. At face value, decentralisation of services into communities seems eminently sensible, and reference centres have been effective in some countries 2Some of these successful schemes are linked to universities that teach community health care and therefore need model community services to train students. The evidence that this approach will work more generally is patchy, and is furthermore based on a series of assumptions that have not been widely tested. The danger in WHO’s strong endorsement of reference centres is that governments and donors may well interpret this as a green light to invest capital in the new service tier. Much more information and research within cities is needed before the architects are called in: the research that WHO are currently coordinating in several cities in Africa and Asia must examine the

assumptions underlying their policy. The WHO strategy is based

the belief that hospitals are often overloaded by patients with minor complaints who should be using cheaper and more basic services. However, there is no firm evidence that hospital overuse is a consistent feature in all countries, and this perception might well reflect overstretched hospital management in certain areas. Large patient throughput in hospitals can undoubtedly give the impression of excessive use if patients spend many hours waiting to be seen or queuing for drugs. Before making global statements about overuse, one needs to on

examine ward throughput and outpatient flow data against the physical and professional resources. Even if hospitals are shown to be overused, WHO policy assumes that the people using hospitals "should" be using the health centres. An alternative view is that hospitals provide a valuable primary health service to people excluded from health centres, which focus services on mothers and children. Adolescents, men, the homeless, and people with sexually transmitted diseases may not feel comfortable in a health centre. The opening of reference centres is no guarantee of an appropriate and accessible service for these population groups. The reference centre policy also assumes that the average cost (ie, per patient seen) of hospital care is greater than the cost at a health centre, and that a reference centre is cheaper than a hospital. Whilst ambulatory surgical care has been shown to be cheaper than hospital care in Cali, Colombia,3such evidence cannot be taken as a general rule. Health centres with a low throughput may have higher average costs than a busy hospital outpatient department. A reference centre functioning as a small hospital with 24-hour cover needs many more staff than a health centre, and this will drive up recurrent costs. Unless the patient throughput per doctor or nurse at a reference centre is higher than that in the hospital, economies of scale suggest that average costs at this new tier will be greater. Few countries can afford increments in their recurrent budget. Yet this additional tier requires staff, drugs, and managerial support. Where should this come from? With about 60-80% of government national health facility expenditure in developing countries absorbed by hospitals,4 an obvious source is existing hospital budgets. If planners intend to trim hospital budgets and reallocate staff to smaller facilities, this strategy must be made explicit from the outset.

Although the reference centre initiative is an important stimulus for planners to evaluate their existing services, there may well be better uses for scarce resources. Capital investment is rarely a solution to complex problems, and the recurrent cost implications may be detrimental to health ministries that are already over-committed. Building a new tier in the health system is a simplistic solution to the broader problems of management and resource

1564

THE LANCET

allocation: countries should not follow the

global call

blindly. The Lancet 1. World Health

Organization. The role of development of urban health systems. WHO

health centres in the Tech Rep Ser 1992; 827:

1-38. 2. World Health

Organization. Improving urban health systems. World Health Stat Q 1991; 44: 234-40. 3. Shepard DS, Walsh J, Munar W, et al. Cost-effectiveness of ambulatory surgery in Cali, Colombia. Presentation at: Outpatient hospitals: their role in health care systems in developing countries. Boston, November, 1990. 4. Mills A. The economics of hospitals in developing countries, part I: expenditure patterns. Health Policy Planning 1990; 5: 107-17.

COMMENTARY DRUG REACTIONS

Sumatriptan and chest pain Clinical studies in over 12 000 patients have confirmed the efficacy of sumatriptan in migraine and cluster headaches.1 This potent and selective 5HTID receptor agonist has predominantly cranial vasoconstrictor effects in animal and human studies and can be given subcutaneously (6 mg) or orally (100 mg). Sensations of heaviness, pressure, and tightness at different sites, including chest and neck, recorded in 3-5 % of patients suggest some extracranial vaspactivity. During early clinical studies, 1 patient experienced cardiac ischaemic events, so a detailed safety programme was initiated (a) to assess the cardiovascular effects; (b) to analyse reports of possible cardiac complications; and (c) to conduct extensive electrocardiographic (ECG) monitoring during trials. Extracranial cardiovascular activity was suggested by increases in blood pressure of 12/10 mm Hg observed 10 min after subcutaneous sumatriptan and lasting for 30-60 min. A lesser effect (7/5 mm Hg) of longer duration was seen with oral therapy. Detailed invasive haemodynamic investigations have now shown increased vascular resistance in both systemic and pulmonary circulations, with an increase in aortic systolic and diastolic pressures of 17-20% and 12-16%, respectively, and a relatively greater rise in pulmonary systolic and diastolic pressures of 40-50% and 33-77%.2,3 The increase in pulmonary capillary wedge pressure by 90% points to additional venoconstrictive effects. These results suggest either that 5HT receptors are more widely distributed than previously recognised or that sumatriptan is less specific in its agonist activity. In-vitro studies in human epicardial arteries confirm 5HT1-like receptor activity. Maximum vasoconstriction following sumatriptan is only 21 % of that seen with 5HT (serotonin). The in-vivo effects were investigated in patients with chest pain but with less than critical coronary artery obstruction After intravenous sumatriptan, mean (stenosis <50%). absolute diameter was reduced by 14 (SD 10)% vs a 16% reduction with subcutaneous administration. There was no ECG evidence of myocardial ischaemia despite symptoms of chest tingling and tightness. When serotonin was given into coronary arteries there was a 52% increase in crosssectional area in normal arteries, a 64% reduction in patients

with angina, and total occlusion in subjects with Prinzmetal angina.4 The reduction in cross-sectional area is at least two-fold greater than with sumatriptan. The ergot alkaloids given therapeutically in migraine have been used as a diagnostic test for coronary artery vasospasm, with a diffuse reduction in arterial diameter of about 30% evident in normal arteries. The vasoconstrictor effect is accentuated with minor arteriosclerotic disease and total occlusion may occur.S In migraineurs, dihydroergotamine therapy has resulted in 18 reported cases of myocardial infarction, with death in 3. 2 patients had a history of cardiac disease. 75% were less than 50 years of age, 83% were women, and 78% had no risk factors for ischaemic heart disease. Thus, the coronary vasoconstrictive effect of sumatriptan seems to be less than that of serotonin or the ergot alkaloid, which show additional 5HT2 and alphareceptor stimulation. Inman and Kubota6 observed patients with chest tightness and suggested that asthma might be induced by sumatriptan. From the clinical database of 75 trials held by Glaxo, who manufacture sumatriptan, 375 asthmatics have been identified who had been treated for 1214 migraine episodes. Only 1 of 6 observed episodes of asthma was believed by the clinical investigators to be related to therapy.6 Chest tightness may indicate stimulation of pulmonary vascular receptors with pulmonary vasoconstriction rather than bronchoconstriction. Coronary vasoconstriction has been suggested by several case-reports but full cardiac investigations have seldom been carried out. Willett et aF reported ST-T wave changes of Prinzmetal character 4 min after subcutaneous sumatriptan in a 47-year-old man. This patient had a history of chest pain, although a negative exercise test had been recorded 75 months before the episode. Underlying obstructive coronary artery disease was not excluded by angiography. Curtin et al8 reported ventricular fibrillation in a 42-year-old woman within 3 min of injection, thought to have been

induced

by

vasospasm.

Subsequent

investigations

confirmed a normal 24 h ECG recording but an exercise test suggested an ischaemic response and coronary arteriography showed a 40% obstructive lesion. This patient had experienced several episodes of palpitations although she was otherwise well.6 Ottervanger et al9 reported a myocardial infarction in a 47-year-old woman after subcutaneous sumatriptan. The ECG showed changes of inferior infarction on admission but strangely no ST elevation; this pattern suggests a previous event or rapid spontaneous coronary artery reperfusion. She had noted chest pain after two previous injections. A subsequent exercise test showed possible ischaemic changes. Of 6124 patients with 28 648 attacks, 2150 had ECGs within 4 h of oral or subcutaneous therapy and 5388 had ECGs at some stage (Glaxo data). Although 4-6% had pressure symptoms, 99% had no ECG changes. Nonspecific changes were seen in 27 (0-5%); new changes of possible myocardial ischaemia occurred in 10 (0-2%) and 5 . were believed to be related to sumatriptan (0-1%). The ECG change was associated with angina in only 1 case. In the subset of oral studies, ECGs were obtained in 1733 of 2786 patients with 24 000 attacks. No irreversible ECG changes were seen, although pressure symptoms occurred in 4-4%. These studies show that the frequency of ECG changes is very low. Overall, there is a small risk of myocardial ischaemia following sumatriptan-induced vasoconstriction. The drug is contraindicated in patients with symptomatic ischaemic