the United Kingdom as soon as possible and should be incorporated into all theatres' control of infection policies. Many health authorities, apparently for financial reasons, are refusing to apply these precautions, even in high risk areas (Chalmers, personal communication). Unfortunately this editorial may help to reinforce the attitude of these authorities. There is now a clear legal requirement to provide protection from microbiological hazards in the health care setting, and the Health and Safety Executive has recently issued the following statement to our association. The Health and Safety at Work etc Act 1974 and the Control of Substances Hazardous to Health Regulations Act 1988 are applicable to the control of microbiological hazards. The Health and Safety Executive has enforced, and will continue to enforce in the future, these legal requirements to ensure that Health Authorities and the managers of units and departments assess the risks to which staff are exposed and take such steps as may be appropriate to remove or control them. We believe that there can be no comparison between the risks to dentists from aerosol contamination and the sometimes massive contamination that can occur when using large power tools, especially saws, and high pressure irrigation systems. The association is therefore recommending that when operating on patients known to be infected with HIV, especially when power tools are being used, additional protection above the universal precautions should be provided, and this may include using ventilated space suits or helmets. The council of the association agrees that at present universal testing is unnecessary. Generally we accept the view put forward by the Royal College of Surgeons of Edinburgh that when a patient is suspected of being infected with HIV then testing should be carried out with the patient's consent.5 If the patient refuses then the case should be considered high risk and additional precautions should be taken. We also believe that any health care worker who sustains a sharps injury should have the right to know whether the patient concerned is infected with HIV. We accept that HIV testing is largely to protect the surgeon and other health care workers, together with their families, but it must not be forgotten that in patients infected with HIV, and especially patients with AIDS, surgery could increase the risk of nosocomial infection. In addition, if HIV infection is diagnosed through testing before surgery then counselling of that patient could help to reduce the spread of the disease in the
community. DAVID HAMBLEN GEOFFREY NEWTON
British Orthopaedic Association, London WC2A 3PN 1 Gazzard BG, Wastell C. HIV and surgeons. BMJ7 1990;301: 1003-4. (3 November.) 2 Centres for Disease Control. Guidelines for prevention of transmission of human immunodeficiency virus and hepatitis B viruses. Atlanta, Georgia, (DC), 1989. 3 American Academy of Orthopaedic Surgeons Task Force. Recommendations for the prevention of human immunodeficiency virus (HIV) transmission in the practice of orthopaedic surgeon. Chicago: AAOS, 1989. 4 United Kingdom Departments of Health. Guidance for clinical health care workers. Recommendations of the expert advisory group on AIDS. London: HMSO, 1990. 5 Royal College of Surgeons of Edinburgh. Statement to Fellows on HIl' infection and AIDS. Edinburgh: Royal College of Surgeons of Edinburgh, 1989.
HIV infection and foreign travel SIR,-We share Dr C J Ellis's anxiety about HIV transmission among travellers but do not agree with his interpretation of the epidemiological data.' He suggests that there is a high risk of infection with HIV and AIDS among heterosexual travellers because of epidemiological data associat-
BMJ
VOLUME 301
24 NOVEMBER 1990
ing infection with exposure abroad. The risk to travellers, however, cannot be inferred from the data because it does not separate out infection in immigrants, refugees, or visitors from infection in United Kingdom residents and because rates cannot be determined as denominator information is lacking. Since 1988 over 85% of patients infected with HIV attending the outpatient department at the Hospital for Tropical Diseases have been immigrants or visitors from African countries and not returning British travellers. We are also concerned that insufficient attention is being paid to the risk of travellers acquiring HIV infection. A prospective survey of travellers conducted in our clinic for advice before travelling showed that most (95%) were aware of the risk factors associated with HIV transmission and understood methods for reducing the risk of infection, such as the use of condoms.2 Only 28% of participants, however, thought that travellers were at greater risk of AIDS because they travelled, and only 25% requested more information on AIDS, even though 30% did not know if AIDS was present in the country they were due to visit. The finding that despite knowledge of sexual transmission of HIV there is no perceived risk of HIV infection associated with travel is of great concern. Information on geographical differences of HIV prevalence may help alter travellers' perception of the risk of HIV infection. If such information is to reach travellers it will need to be provided through travel agents as many people do not seek health advice before travelling.3 All organisations concerned with travel need to increase education about AIDS and make all travellers more aware of the risks of acquiring HIV infection while abroad. R H BEHRENS
Hospital for Tropical Diseases, London NW1
J D H PORTER Communicable Disease Surveillance Centre, London NW9 5EQ 1 Ellis CJ. HIV infection and travel. BMJ7 1990;301:984-5. (27 October.) 2 Porter JDH, Phillips-Howard PA, Behrens RH. AIDS awareness among travellers. Travel Medicine International (in press). 3 Cossar JH, Reid D. Health hazards of international travel. World Health Stat Qu 1989;42:61-9.
Aerobic work capacity in chronic fatigue syndrome SIR,-The data of Dr Marshall S Riley and colleagues' are consistent with our findings2 that most patients referred with the chronic fatigue syndrome have the effort syndrome-that is, chronic hyperventilation as a consequence of excessive effort and distress.3 May we draw attention to three points. Dr Riley and colleagues concluded that the patients could not be hyperventilating because their values of end-tidal partial pressure of carbon dioxide at rest and at peak exercise did not differ significantly from those of the controls. In our opinion the values published for the controls (35 8 mmHg at rest and 36-3 mmHg at peak exercise) are too low to be accepted as normal. The finding that the patients reached their anaerobic threshold far quicker than did the controls is consistent with the early acidosis on exertion known to occur in chronic hyperventilation. This is a consequence of the depletion of the body's buffer base reserves,4 brought about by renal compensation for chronic respiratory alkalosis.5 In their patients the disturbance of perception was an overestimate of loss of capacity for effort compared with controls. In many of our patients we believe that a failure of perception of effort and distress might have contributed to them pushing themselves so deeply into ill health. Failure to perceive hypocapnia is a characteristic
of patients with chronic fatigue and creates an appreciable therapeutic problem.6 S D ROSEN J C KING
J B WILKINSON P G F NIXON
Charing Cross Hospital, London W6 8RF
1 Riley MS, O'Brien CJ, McCluskey DR, Bell NP, Nicholls DP. Aerobic work capacity in patients with chronic fatigue syndrome. BMJ 1990;301:953-6. 2 Rosen SD, King JC, Nixon PGF. Is chronic fatigue syndrome synonymous with effort syndrome?J7 R Soc Med (in press). 3 Soley MH, Shock MW. The aetiology of effort syndrome.
AmJMedSci 1938;196:840-51.
4 Lewis T, Cotton C, Barcroft J, Milroy TR, Dufton D, Parsons
TR. Breathlessness in soldiers suffering from irritable heart. BMJ 1916;ii:517-9. 5 Gennari FH, Goldstein MB, Schwartz WB. The nature of
the renal adaptation to chronic hypocapnia. J Clin Invest 1972;51: 1722-30. 6 King JC, Rosen SD, Nixon PGF. Failure of perception of hypocapnia: physiological and clinical implications. J R Soc Med (in press).
AUTHOR'S REPLY,-Hyperventilation is a well recognised condition that, by definition, is associated with a low end tidal partial pressure of carbon dioxide (PETCo2). Although we did not measure the PETCo2 during the recovery phase of the exercise testing, values obtained for controls and patients with the chronic fatigue syndrome before exercise and during the treadmill testing for patients with the chronic fatigue syndrome were not significantly different from values for control subjects or patients with the irritable bowel syndrome. All the patients with the chronic fatigue syndrome were symptomatic at the time of exercise testing, and if the syndrome is due entirely to hyperventilation then we would have expected to find some appreciable abnormality in this value. Since the PETco2 value of these patients did not significantly differ from that of the two control populations, irrespective of the absolute values, which may be lower than expected for methodological reasons, we would be confident that the group with the chronic fatigue syndrome that we studied did not hyperventilate. Dr Rosen and colleagues rightly observe that the patients with the chronic fatigue syndrome reached their anaerobic threshold more quickly than did the control subjects. Though this is consistent with early acidosis on exertion, which may occur in patients who hyperventilate, it is also consistent with deconditioning of muscle. The finding of a high resting heart rate and significantly faster heart rates at submaximal exertion would indicate that these subjects had become less physically fit and makes the second explanation more likely. We cannot accept that the clinical features of the syndrome or the reduced exercise capacity of patients with this condition can be explained by hyperventilation. D R McCLUSKEY
Institute of Clinical Science, Belfast BS12 6RJ
Interventions in chronic renal failure SIR,-It is disappointing that the review by Dr J R Curtis on the progression of chronic renal failure' should concentrate so heavily on the hyperfiltration hypothesis. This theory, that hyperfiltration and glomerular hypertension play a causative part in the progressive glomerulosclerosis that follows renal ablation in rats -and therefore perhaps also in the similar process that occurs after loss of functioning renal tissue in humans-certainly dominated the 1980s, but recent work casts doubt on the cause and effect relation.2` Serial micropuncture analysis has shown no correlation between the extent of structural damage and
1217
the degree of hyperfiltration and glomerular hypertension. Studies using different antihypertensive regimens after renal ablation in rats have shown that comparable reductions in systemic blood pressure provide similar protection against glomerulosclerosis irrespective of the effect on glomerular pressure and hyperfiltration.3 Considerable protection against glomerulosclerosis is also provided by inhibition of thromboxane synthesis4 or treatment with heparin,5 in each case without affecting hyperfiltration or glomerular hypertension. The effect of heparin is independent of its anticoagulant properties as similar protection can be achieved with a low molecular weight nonanticoagulant form of the molecule.9 Increases in mesangial cell number and mesangial matrix production are prominent features in progressive glomerulosclerosis: heparin is a potent inhibitor of mesangial cell proliferation and matrix production in vitro, and again this effect can be reproduced with the non-anticoagulant form of the molecule.7 A further area of recent research is the role of peptide growth factors in the adaptation to loss of renal mass. Intrarenal production of insulin-like growth factor type 1 increases after contralateral nephrectomy,5 and this growth factor has mitogenic effects on renal cells in vitro.9 Other growth factors, such as platelet derived growth factor, have potent mitogenic effects on mesangial cells in vitro,"' but their role in vivo has yet to be characterised. Current attempts at intervention in progressive chronic renal failure have been designed on the basis of the hyperfiltration hypothesis. The deficiencies of the hypothesis may partly explain the relative lack of success of such attempts. It is to be hoped that recent advances in understanding the cellular mechanisms underlying progressive glomerulosclerosis may lead to the development of more rational and therefore more effective treatments. P W MATHIESON
Department of Medicine, Addenbrooke's Hospital, Cambridge CB2 2QQ I Ctirtis JR. Interventions in chronic renal failure. 301:622-4. (29 September.)
BMJ7 1990;
2 Yoshida Y, Fogo A, Shiraga H, Glick AD, Ichikawa I. Serial micropuncture analysis of single nephron function in subtotal renal ablation. Kidney Int 1988;33:855-67. 3 Yoshida Y, Kawamura T, Ikoma M, Fogo A, Ichikawa I. Et'fects of antihypertensive druLgs on glomerular morphology.
Kidney Int 1989;36:626-35.
4 Salvati P, Ferti C, Ferrario RG, et al. Role of enhanced glomerular synthesis of thromboxane A, in progressive kidney disease. Kidnes' Int 1990;38:447-58. S Ichikawa I, Yoshida Y, Fogo A, Purkerson MNIL, Klahr S. Effect of heparin on the glomerular structure and function of remnant nephrons. Kidtney Int 1988;34:638-44. 6 Purkersot Ml., ,T'ollefsen l)M, KlahrS. N-desulfated/acetylated heparin ameliorates the progression of renal disease in rats with subtotal renal ablation.] Clin Invest 1988;81:69-74. 7 Castellot JJ Jr, Hoover RI., Harper PA, Karnovsky MJ.
Heparin and glomerular cpithelial cell-secreted heparinlike species inhibit mesangial cell proliferation. Am 7 Pathol 1985;120:427-35. 8 Fagin JA, Melmed S. Relative increase in insulin-like growth factor I messenger ribonucleic acid levels in compensatory renal hypertrophy. Endocrinology 1987;120:718-24. 9 Segal R, Fine LG. Polypeptide growth factors and the kidney. Kidney Int 1989;36(suppl 27):S2-10. 10 Silver BJ, Jaffer FE, Abboud HE. Platelet-derived growth factor synthesis in mesangial cells: induction by multiple peptide mitogens. Proc Natl.Acad Sci USA 1989;86:1056-60.
Pressure for no fault on three fronts SIR,-Ms Clare Dyer writes about the pressure for a no fault compensation scheme.' It seems to me that although many people have argued the advantages of no fault liability, few have commented on its disadvantages. Other no fault schemes exclude sickness, disease, or the aging process because they are not encompassed in the definition of an accident. It may be
1218
difficult to ascertain whether an event is tle result of an accident in a medical context because there may be many reasons why it occurred. Similarly, as the scheme would be state funded the definition may be restricted by political decisions or due to financial resources. Failure to treat or to diagnose may also not be compensated because the harm would have arisen from the original disease. Even worse, the person harmed would have no recourse to a civil action. It may even be argued that not being allowed to sue is an infringement of human rights. Failure of information disclosure (that is, giving informed consent) is also not covered, and so all that is unethical about "paternalistic" medicine would re-emerge. No fault schemes in other countries such as Sweden and New Zealand are backed by a very comprehensive social security system, so that the compensation received is essentially only a top up. Britain would have to invest heavily in its social security before any no fault scheme would be effective. N PACE
Milngavie, Glasgow G62 7JD 1 Dver C. Pressure for no fault on three fronts. BMJ7 1990;301: 1010-1. (3 November.)
submit that the most important are not included. Though we support the undertaking and publishing of research on this important topic, we must conclude that the results fail to support the conclusion that patients prefer their doctors to be directive. PAUL KINNERSLEY PENELOPE OWEN JONATHAN RICHARDS CLARE WILKINSON
University of Wales College of Medicine, Llanedeyrn, Cardiff CF3 7PN 1 Savage R, Armstrong D. Effect of a general practitioner's consulting style on patients' satisfaction: a controlled study. BM,J 1990;301:%8-9. (27 October.) 2 McWhinney IR. A textbook offamily medicine. Oxford: Oxford University Press, 1989:111-52. 3 Neighbour R. The inner consultation. Lancaster: MTP Press, 1987:15 1-82. 4 Levenstein JH, McCracken EC, McWhinney IR, Stewart MA, Brown JB. The patient-centred clinical method. 1. A model for the doctor-patient interaction in family medicine. Fam Pract 1986;3:24-30. 5 Byrne PS, Long BEL. Doctors talking to patients. London: HMSO, 1976. 6 Tuckett D, Boulton M, Olsen C, Williams A. Meetings between experts: an approach to sharing ideas in medical consultations. London: Tavistock, 1985. 7 Henbest RJ, Stewart M. Patient-centredness in the consultation. 2: Does it really make a difference? Fam Pract 1990;7:28-33. 8 Henbest RJ. A study of the patient centred approach in family medicine [MCISc thesis]. Ontario: University of Ontario, 1985.
Effect of a general practitioner's Please think again, Mr consulting style Waldegrave
SIR, -We consider the recent paper by Drs Richard Savage and David Armstrong to be philosophically and methodologically flawed.' McWhinney2 and other researchers3'5 have described and studied the patient centred clinical model; a process in which the doctors' and the patients' parallel agendas are searched. The consultation includes integration and summarising aimed at reconciling these two agendas. This is a broader and more complex perspective of the consultation than the simple dichotomous model presented by Drs Savage and Armstrong. The examples given of a "sharing" style are interrogative questions rather than a more complete representation of the definition of a sharing style.6 The title and abstract of the paper do not make it clear that the authors mainly make their claims for a directive style in the context of giving information and treatment for physical illness, and therefore could mislead many readers. Studies have shown that patient centred care was positively and significantly associated with resolution of concern, symptom resolution, and the degree to which the patient felt understood.78 The authors concluded that doctor's style is only one aspect of patient centredness, which in turn is only one component of the developing personal relationship between doctor and patient. Dr Savage was the only doctor observed in this study; he will have an established style of consulting and his patients will be accustomed to this style. His observation about the importance of consistency suggests that he normally consults in a directive manner. Patients who preferred a different style may have chosen to consult other doctors in the practice. Therefore, when Dr Savage "changed" his style at the point of randomisation patients were, unsurprisingly, less satisfied with the consultation. Whether an individual doctor can randomise his skills needs scientific validation in the light of research that suggests that a doctor's style is usually consistent.5 The results would be less likely to be biased if he had consulted with a group of patients with no predetermined expectations-for example, by conducting the study in a different practice while acting as a locum. Although the authors mention a number of potential sources of error in their discussion, we
SIR, -Scrutator reports that some health authorities have no medical representation and refuse to recognise medical advisory committees.' Guy's and Lewisham Hospitals were the first in the United Kingdom to adopt a system of medical management in which clinical directors were appointed, with the consent of their colleagues, to serve on management boards responsible for running the hospitals. We have therefore had several years' experience of the system. At both hospitals the medical committee has been retained, and it meets three or four times a year, giving all consultants the opportunity to express their individual and collective opinions. It can search out information and set up its own select committees to examine important issues in depth, and its chairman is a member of the management board. In this respect, however, the purpose of the medical committee is not to manage but to monitor management. It is, in a sense, a parliamentary body, which gains its power and authority from the breadth of its consultant membership. In our hospitals the medical committee is not an alternative to the management board; it is independent of the board and a vitally important component of the system, giving the system a greater strength than it would otherwise have. We are concerned to hear that some other hospitals that are adopting the directorate system are seriously considering disbanding their medical committees. We would advise them to think twice before doing so. NORMAN ALAN SIMMONS CYRIL CHANTLER
GORDON JACKSON HARRY KEEN ROBIN STOTT
Guy's Hospital, London SEI 9RT 1 Anonymous. Please think again, Mr Clarke. BMJ 1990;301:834.
(13 October.)
General practitioner fundholding SIR, -We are told that fundholding practices will be bad for patients in general. The recent local medical committee conference passed a vote
BMJ
VOLUME
301
24
NOVEMBER
1990
community. DAVID HAMBLEN GEOFFREY NEWTON
British Orthopaedic Association, London WC2A 3PN 1 Gazzard BG, Wastell C. HIV and surgeons. BMJ7 1990;301: 1003-4. (3 November.) 2 Centres for Disease Control. Guidelines for prevention of transmission of human immunodeficiency virus and hepatitis B viruses. Atlanta, Georgia, (DC), 1989. 3 American Academy of Orthopaedic Surgeons Task Force. Recommendations for the prevention of human immunodeficiency virus (HIV) transmission in the practice of orthopaedic surgeon. Chicago: AAOS, 1989. 4 United Kingdom Departments of Health. Guidance for clinical health care workers. Recommendations of the expert advisory group on AIDS. London: HMSO, 1990. 5 Royal College of Surgeons of Edinburgh. Statement to Fellows on HIl' infection and AIDS. Edinburgh: Royal College of Surgeons of Edinburgh, 1989.
HIV infection and foreign travel SIR,-We share Dr C J Ellis's anxiety about HIV transmission among travellers but do not agree with his interpretation of the epidemiological data.' He suggests that there is a high risk of infection with HIV and AIDS among heterosexual travellers because of epidemiological data associat-
BMJ
VOLUME 301
24 NOVEMBER 1990
ing infection with exposure abroad. The risk to travellers, however, cannot be inferred from the data because it does not separate out infection in immigrants, refugees, or visitors from infection in United Kingdom residents and because rates cannot be determined as denominator information is lacking. Since 1988 over 85% of patients infected with HIV attending the outpatient department at the Hospital for Tropical Diseases have been immigrants or visitors from African countries and not returning British travellers. We are also concerned that insufficient attention is being paid to the risk of travellers acquiring HIV infection. A prospective survey of travellers conducted in our clinic for advice before travelling showed that most (95%) were aware of the risk factors associated with HIV transmission and understood methods for reducing the risk of infection, such as the use of condoms.2 Only 28% of participants, however, thought that travellers were at greater risk of AIDS because they travelled, and only 25% requested more information on AIDS, even though 30% did not know if AIDS was present in the country they were due to visit. The finding that despite knowledge of sexual transmission of HIV there is no perceived risk of HIV infection associated with travel is of great concern. Information on geographical differences of HIV prevalence may help alter travellers' perception of the risk of HIV infection. If such information is to reach travellers it will need to be provided through travel agents as many people do not seek health advice before travelling.3 All organisations concerned with travel need to increase education about AIDS and make all travellers more aware of the risks of acquiring HIV infection while abroad. R H BEHRENS
Hospital for Tropical Diseases, London NW1
J D H PORTER Communicable Disease Surveillance Centre, London NW9 5EQ 1 Ellis CJ. HIV infection and travel. BMJ7 1990;301:984-5. (27 October.) 2 Porter JDH, Phillips-Howard PA, Behrens RH. AIDS awareness among travellers. Travel Medicine International (in press). 3 Cossar JH, Reid D. Health hazards of international travel. World Health Stat Qu 1989;42:61-9.
Aerobic work capacity in chronic fatigue syndrome SIR,-The data of Dr Marshall S Riley and colleagues' are consistent with our findings2 that most patients referred with the chronic fatigue syndrome have the effort syndrome-that is, chronic hyperventilation as a consequence of excessive effort and distress.3 May we draw attention to three points. Dr Riley and colleagues concluded that the patients could not be hyperventilating because their values of end-tidal partial pressure of carbon dioxide at rest and at peak exercise did not differ significantly from those of the controls. In our opinion the values published for the controls (35 8 mmHg at rest and 36-3 mmHg at peak exercise) are too low to be accepted as normal. The finding that the patients reached their anaerobic threshold far quicker than did the controls is consistent with the early acidosis on exertion known to occur in chronic hyperventilation. This is a consequence of the depletion of the body's buffer base reserves,4 brought about by renal compensation for chronic respiratory alkalosis.5 In their patients the disturbance of perception was an overestimate of loss of capacity for effort compared with controls. In many of our patients we believe that a failure of perception of effort and distress might have contributed to them pushing themselves so deeply into ill health. Failure to perceive hypocapnia is a characteristic
of patients with chronic fatigue and creates an appreciable therapeutic problem.6 S D ROSEN J C KING
J B WILKINSON P G F NIXON
Charing Cross Hospital, London W6 8RF
1 Riley MS, O'Brien CJ, McCluskey DR, Bell NP, Nicholls DP. Aerobic work capacity in patients with chronic fatigue syndrome. BMJ 1990;301:953-6. 2 Rosen SD, King JC, Nixon PGF. Is chronic fatigue syndrome synonymous with effort syndrome?J7 R Soc Med (in press). 3 Soley MH, Shock MW. The aetiology of effort syndrome.
AmJMedSci 1938;196:840-51.
4 Lewis T, Cotton C, Barcroft J, Milroy TR, Dufton D, Parsons
TR. Breathlessness in soldiers suffering from irritable heart. BMJ 1916;ii:517-9. 5 Gennari FH, Goldstein MB, Schwartz WB. The nature of
the renal adaptation to chronic hypocapnia. J Clin Invest 1972;51: 1722-30. 6 King JC, Rosen SD, Nixon PGF. Failure of perception of hypocapnia: physiological and clinical implications. J R Soc Med (in press).
AUTHOR'S REPLY,-Hyperventilation is a well recognised condition that, by definition, is associated with a low end tidal partial pressure of carbon dioxide (PETCo2). Although we did not measure the PETCo2 during the recovery phase of the exercise testing, values obtained for controls and patients with the chronic fatigue syndrome before exercise and during the treadmill testing for patients with the chronic fatigue syndrome were not significantly different from values for control subjects or patients with the irritable bowel syndrome. All the patients with the chronic fatigue syndrome were symptomatic at the time of exercise testing, and if the syndrome is due entirely to hyperventilation then we would have expected to find some appreciable abnormality in this value. Since the PETco2 value of these patients did not significantly differ from that of the two control populations, irrespective of the absolute values, which may be lower than expected for methodological reasons, we would be confident that the group with the chronic fatigue syndrome that we studied did not hyperventilate. Dr Rosen and colleagues rightly observe that the patients with the chronic fatigue syndrome reached their anaerobic threshold more quickly than did the control subjects. Though this is consistent with early acidosis on exertion, which may occur in patients who hyperventilate, it is also consistent with deconditioning of muscle. The finding of a high resting heart rate and significantly faster heart rates at submaximal exertion would indicate that these subjects had become less physically fit and makes the second explanation more likely. We cannot accept that the clinical features of the syndrome or the reduced exercise capacity of patients with this condition can be explained by hyperventilation. D R McCLUSKEY
Institute of Clinical Science, Belfast BS12 6RJ
Interventions in chronic renal failure SIR,-It is disappointing that the review by Dr J R Curtis on the progression of chronic renal failure' should concentrate so heavily on the hyperfiltration hypothesis. This theory, that hyperfiltration and glomerular hypertension play a causative part in the progressive glomerulosclerosis that follows renal ablation in rats -and therefore perhaps also in the similar process that occurs after loss of functioning renal tissue in humans-certainly dominated the 1980s, but recent work casts doubt on the cause and effect relation.2` Serial micropuncture analysis has shown no correlation between the extent of structural damage and
1217
the degree of hyperfiltration and glomerular hypertension. Studies using different antihypertensive regimens after renal ablation in rats have shown that comparable reductions in systemic blood pressure provide similar protection against glomerulosclerosis irrespective of the effect on glomerular pressure and hyperfiltration.3 Considerable protection against glomerulosclerosis is also provided by inhibition of thromboxane synthesis4 or treatment with heparin,5 in each case without affecting hyperfiltration or glomerular hypertension. The effect of heparin is independent of its anticoagulant properties as similar protection can be achieved with a low molecular weight nonanticoagulant form of the molecule.9 Increases in mesangial cell number and mesangial matrix production are prominent features in progressive glomerulosclerosis: heparin is a potent inhibitor of mesangial cell proliferation and matrix production in vitro, and again this effect can be reproduced with the non-anticoagulant form of the molecule.7 A further area of recent research is the role of peptide growth factors in the adaptation to loss of renal mass. Intrarenal production of insulin-like growth factor type 1 increases after contralateral nephrectomy,5 and this growth factor has mitogenic effects on renal cells in vitro.9 Other growth factors, such as platelet derived growth factor, have potent mitogenic effects on mesangial cells in vitro,"' but their role in vivo has yet to be characterised. Current attempts at intervention in progressive chronic renal failure have been designed on the basis of the hyperfiltration hypothesis. The deficiencies of the hypothesis may partly explain the relative lack of success of such attempts. It is to be hoped that recent advances in understanding the cellular mechanisms underlying progressive glomerulosclerosis may lead to the development of more rational and therefore more effective treatments. P W MATHIESON
Department of Medicine, Addenbrooke's Hospital, Cambridge CB2 2QQ I Ctirtis JR. Interventions in chronic renal failure. 301:622-4. (29 September.)
BMJ7 1990;
2 Yoshida Y, Fogo A, Shiraga H, Glick AD, Ichikawa I. Serial micropuncture analysis of single nephron function in subtotal renal ablation. Kidney Int 1988;33:855-67. 3 Yoshida Y, Kawamura T, Ikoma M, Fogo A, Ichikawa I. Et'fects of antihypertensive druLgs on glomerular morphology.
Kidney Int 1989;36:626-35.
4 Salvati P, Ferti C, Ferrario RG, et al. Role of enhanced glomerular synthesis of thromboxane A, in progressive kidney disease. Kidnes' Int 1990;38:447-58. S Ichikawa I, Yoshida Y, Fogo A, Purkerson MNIL, Klahr S. Effect of heparin on the glomerular structure and function of remnant nephrons. Kidtney Int 1988;34:638-44. 6 Purkersot Ml., ,T'ollefsen l)M, KlahrS. N-desulfated/acetylated heparin ameliorates the progression of renal disease in rats with subtotal renal ablation.] Clin Invest 1988;81:69-74. 7 Castellot JJ Jr, Hoover RI., Harper PA, Karnovsky MJ.
Heparin and glomerular cpithelial cell-secreted heparinlike species inhibit mesangial cell proliferation. Am 7 Pathol 1985;120:427-35. 8 Fagin JA, Melmed S. Relative increase in insulin-like growth factor I messenger ribonucleic acid levels in compensatory renal hypertrophy. Endocrinology 1987;120:718-24. 9 Segal R, Fine LG. Polypeptide growth factors and the kidney. Kidney Int 1989;36(suppl 27):S2-10. 10 Silver BJ, Jaffer FE, Abboud HE. Platelet-derived growth factor synthesis in mesangial cells: induction by multiple peptide mitogens. Proc Natl.Acad Sci USA 1989;86:1056-60.
Pressure for no fault on three fronts SIR,-Ms Clare Dyer writes about the pressure for a no fault compensation scheme.' It seems to me that although many people have argued the advantages of no fault liability, few have commented on its disadvantages. Other no fault schemes exclude sickness, disease, or the aging process because they are not encompassed in the definition of an accident. It may be
1218
difficult to ascertain whether an event is tle result of an accident in a medical context because there may be many reasons why it occurred. Similarly, as the scheme would be state funded the definition may be restricted by political decisions or due to financial resources. Failure to treat or to diagnose may also not be compensated because the harm would have arisen from the original disease. Even worse, the person harmed would have no recourse to a civil action. It may even be argued that not being allowed to sue is an infringement of human rights. Failure of information disclosure (that is, giving informed consent) is also not covered, and so all that is unethical about "paternalistic" medicine would re-emerge. No fault schemes in other countries such as Sweden and New Zealand are backed by a very comprehensive social security system, so that the compensation received is essentially only a top up. Britain would have to invest heavily in its social security before any no fault scheme would be effective. N PACE
Milngavie, Glasgow G62 7JD 1 Dver C. Pressure for no fault on three fronts. BMJ7 1990;301: 1010-1. (3 November.)
submit that the most important are not included. Though we support the undertaking and publishing of research on this important topic, we must conclude that the results fail to support the conclusion that patients prefer their doctors to be directive. PAUL KINNERSLEY PENELOPE OWEN JONATHAN RICHARDS CLARE WILKINSON
University of Wales College of Medicine, Llanedeyrn, Cardiff CF3 7PN 1 Savage R, Armstrong D. Effect of a general practitioner's consulting style on patients' satisfaction: a controlled study. BM,J 1990;301:%8-9. (27 October.) 2 McWhinney IR. A textbook offamily medicine. Oxford: Oxford University Press, 1989:111-52. 3 Neighbour R. The inner consultation. Lancaster: MTP Press, 1987:15 1-82. 4 Levenstein JH, McCracken EC, McWhinney IR, Stewart MA, Brown JB. The patient-centred clinical method. 1. A model for the doctor-patient interaction in family medicine. Fam Pract 1986;3:24-30. 5 Byrne PS, Long BEL. Doctors talking to patients. London: HMSO, 1976. 6 Tuckett D, Boulton M, Olsen C, Williams A. Meetings between experts: an approach to sharing ideas in medical consultations. London: Tavistock, 1985. 7 Henbest RJ, Stewart M. Patient-centredness in the consultation. 2: Does it really make a difference? Fam Pract 1990;7:28-33. 8 Henbest RJ. A study of the patient centred approach in family medicine [MCISc thesis]. Ontario: University of Ontario, 1985.
Effect of a general practitioner's Please think again, Mr consulting style Waldegrave
SIR, -We consider the recent paper by Drs Richard Savage and David Armstrong to be philosophically and methodologically flawed.' McWhinney2 and other researchers3'5 have described and studied the patient centred clinical model; a process in which the doctors' and the patients' parallel agendas are searched. The consultation includes integration and summarising aimed at reconciling these two agendas. This is a broader and more complex perspective of the consultation than the simple dichotomous model presented by Drs Savage and Armstrong. The examples given of a "sharing" style are interrogative questions rather than a more complete representation of the definition of a sharing style.6 The title and abstract of the paper do not make it clear that the authors mainly make their claims for a directive style in the context of giving information and treatment for physical illness, and therefore could mislead many readers. Studies have shown that patient centred care was positively and significantly associated with resolution of concern, symptom resolution, and the degree to which the patient felt understood.78 The authors concluded that doctor's style is only one aspect of patient centredness, which in turn is only one component of the developing personal relationship between doctor and patient. Dr Savage was the only doctor observed in this study; he will have an established style of consulting and his patients will be accustomed to this style. His observation about the importance of consistency suggests that he normally consults in a directive manner. Patients who preferred a different style may have chosen to consult other doctors in the practice. Therefore, when Dr Savage "changed" his style at the point of randomisation patients were, unsurprisingly, less satisfied with the consultation. Whether an individual doctor can randomise his skills needs scientific validation in the light of research that suggests that a doctor's style is usually consistent.5 The results would be less likely to be biased if he had consulted with a group of patients with no predetermined expectations-for example, by conducting the study in a different practice while acting as a locum. Although the authors mention a number of potential sources of error in their discussion, we
SIR, -Scrutator reports that some health authorities have no medical representation and refuse to recognise medical advisory committees.' Guy's and Lewisham Hospitals were the first in the United Kingdom to adopt a system of medical management in which clinical directors were appointed, with the consent of their colleagues, to serve on management boards responsible for running the hospitals. We have therefore had several years' experience of the system. At both hospitals the medical committee has been retained, and it meets three or four times a year, giving all consultants the opportunity to express their individual and collective opinions. It can search out information and set up its own select committees to examine important issues in depth, and its chairman is a member of the management board. In this respect, however, the purpose of the medical committee is not to manage but to monitor management. It is, in a sense, a parliamentary body, which gains its power and authority from the breadth of its consultant membership. In our hospitals the medical committee is not an alternative to the management board; it is independent of the board and a vitally important component of the system, giving the system a greater strength than it would otherwise have. We are concerned to hear that some other hospitals that are adopting the directorate system are seriously considering disbanding their medical committees. We would advise them to think twice before doing so. NORMAN ALAN SIMMONS CYRIL CHANTLER
GORDON JACKSON HARRY KEEN ROBIN STOTT
Guy's Hospital, London SEI 9RT 1 Anonymous. Please think again, Mr Clarke. BMJ 1990;301:834.
(13 October.)
General practitioner fundholding SIR, -We are told that fundholding practices will be bad for patients in general. The recent local medical committee conference passed a vote
BMJ
VOLUME
301
24
NOVEMBER
1990
