BRITISH MEDICAL JOURNAL
18 MARCH 1978
itself in the colon and then secrete an exotoxin with a necrotising effect on the colonic mucosa. Clearly the organism must be highly sensitive to vancomycin and non-absorbable sulphonamides. The new tools, then, in our management of pseudomembranous colitis are the screening test for toxin in the stools or in biopsy specimens; careful stool culture for pathogens; and the specific treatment with vancomycin. But we need to know whether other organisms and other toxins are concerned, and which antibiotics may be used to combat them. lDearing, W H, et al, Gastroenterology, 1954, 26, 38. 2Speare, G S, AmericantJouirnal of Suirgery, 1954, 88, 523. 3Bartlett, J G, and Gorbach, S L, Advances in Internal Medicine, 1977, 22, 455. 4Ecker, J A, et al, Amtiericani Yoturtnal of Gastroenterology, 1970, 54, 214. 5British Medical Journal, 1974, 4, 65. Miller, R R, and Hershel, J, Clinical Phlarnmacology anid Therapeutics, 1977, 22, 1. Tedesco, F J, et al, Annals of Inzternal Medicine, 1974, 81, 429. Buts, J P, et al, Gastroenterology, 1977, 73, 823. 9Price, A B, and Davies, D R, Youirnal of Clinical Pathology, 1977, 30, 1. Goodman, M J, and Truclove, S C, British Medical3Journal, 1976, 3, 354. L arson, H E, et al, British Medical Journal, 1977, 1, 1246. ' Rifkin, G D, et al, Lanicet, 1977, 2, 1103. 13 ILarson, H E, and Price, A B, Lancet, 1977, 2, 1312. " Small, J D, Laboratory Anlimal Care, 1968, 18, 411. 15 Bartlett. J G, ct al, Gastroenterology, 1977, 73, 772. "' Bartlett, J G, et al, Lancet, 1978, 1, 338.
Knowing the oxygenation of the fetus About half of all stillbirths are accounted for by infants who die, often during labour, with no discernible cause of death except "anoxia." While this diagnosis may be unhelpful as a basis for understanding primary causes, it has focused obstetricians' attention on a mode of death which should often be preventable. If during labour a fetus is known to be suffering lack of oxygen then rapid delivery and resuscitation may be lifesaving: indeed, these may save more than its life, since degrees of hypoxia which are not fatal seem likely to cause cerebral damage, and intellectual impairment of children may well be a much larger problem than perinatal death. The technological aspects of monitoring fetal wellbeing have evolved as part of the modern concept of intensive care applied to the fetuses of pregnant women thought to be at special risk. Nevertheless, the measurement of fetal oxygenation has proved technically elusive, and for the past 20 years the two most common approaches to the problem have been indirect. One has been to study fetal heart rate patterns, which are influenced by hypoxia, among other things; the other to study blood samples obtained from the fetal scalp, when acidosis (as indicated by the pH) has been the most used indicator of fetal hypoxia. While both techniques have made substantial contributions to perinatal care and fetal salvage, they have major shortcomings. The huge numbers of reports on fetal heart rate patterns have shown that they may change for many reasons apart from hypoxia,2 and the analysis and interpretation of these patterns are now considered so complex that resort has been made to computer analysis.3 Clearly, estimation of the pH in fetal scalp blood is a closer approach to fetal oxygenation, and some4 consider that abnormal fetal heart rate patterns are difficult to interpret without knowing the pH. But a fall in pH is a relatively late effect of hypoxia, and the intermittent
671
nature of blood sampling-a techi ique with its own hazardsmeans that hypoxia of rapid ons-L may not be detected in time. Ideally the obstetrician would like to have a direct and continuous record of fetal oxygen tension, and that ideal now seems to be within reach. The first supplement to be published by the British Journal of Obstetrics and Gynaecology5 presents the accumulated experience of a German and a Swedish team who have pioneered continuous transcutaneous monitoring of fetal oxygen tension in labour using a Clark type electrode fixed to the fetal scalp. Technical development of the electrode has resulted in one small enough to be applied through a cervix at least 3 cm dilated. It is fixed to the skin with a tissue glue, and an integral heater raises the temperature of the area below the electrode to 44°C for effective vasodilatation. Within 20 minutes a continuous record of Po, is available, and experience suggests that recordings for more than four hours are quite feasible. One of the most enlightening aspects of this report is the association between transcutaneous P02 levels and simultaneously recorded fetal heart rate patterns. The sinister implications of severe late decelerations were confirmed: in these circumstances the Po2 was always below 15 mm Hg, and similar Po, levels were associated with basal fetal heart rates of under 100 and over 180. Unexpectedly, loss of baseline variability of fetal heart rate was not always associated with a low P02. A further striking finding was the way in which supplementary oxygen given to the mother could raise the fetal Po0, and the way in which maternal apnoea after hyperventilation in labour could result in a dangerous fall in fetal P02. In transcutaneous monitoring perinatal medicine has a new and powerful tool, and both perinatal research and fetal clinical care should benefit. 1 Chamberlain, R, British Births, 1970, vol 1. London, Heinemann, 1975. 2 Ott, W J, Obstetrical and Gynecological Survey, 1976, 31, 339. Thomas, C, and Blackwell, R J, British J7ournal of Obstetrics and Gynaecology, 1975, 82, 634. 4 Beard, R W, Pediatrics, 1974, 53, 157. 5 Huch, A, et al, British J7ournal of Obstetrics and Gynaecology, 1977, 84, suppl 1.
What kind of cot death? Local studies of postneonatal mortality1 2 are gradually confirming the important point, made first by Sheffield researchers,3 that sudden unexpected deaths at home are a "mixed bag." We are beginning to recognise three categories: the baby whose acute infective illness is underestimated by health teams or parents and therefore does not receive the benefit of modern paediatric care; the baby who has an apparently minor illness which in some way triggers sudden death; and the baby who clinically and pathologically appears to have been well. This heterogeneity reduces the value of the epidemiological facts about cot death that continue to be gathered-age distribution, sex difference, seasonal variation, day of week and time of day found dead, mother's age, size of family, birth weight, length of gestation, complications of labour and delivery, method of feeding, mother's blood group, parental smoking, socioeconomic status of the family and of the geographical area, and the baby's level of activity and behaviour from birth.10 No study has attempted to differentiate its findings for the three clinicopathological categories of cot
BRITISH MEDICAL JOURNAL
672
death, usually because small numbers have made this impossible. Until this has been done, however, it is hard to see a logical application for the at-risk scoring concept proposed by the Sheffield group.11 12 A further problem with the Sheffield system is that in its existing form it does not seem to predict death as accurately in other cities.13 What, then, are the current prospects for preventing cot deaths ? For the first group-those who die from rapidly progressing and inadequately recognised infective illnessthere are clear preventive possibilities in improving the accessibility of health services for young children and in better training for doctors and nurses in recognising life-threatening paediatric conditions. Lasting progress seems more likely to come from organisational and training changes, embodying the spirit if not the letter of the Court proposals,14 than from specific measures directed at families with multiple "risk factors." If minor illnesses are important triggers of sudden death in the second group of cot deaths then improvements in general living conditions may be more important than health services. A large part of the explanation for the low incidence of cot death in countries such as Sweden may be related to housing, population density, and other special factors. Babies in the third group, who die without any observable illness, remain the most difficult problem. We have growing evidence that the mechanism of death may be apnoea similar to that seen in premature babies,15-20 but even on the rare occasions when it has been possible to identify babies at risk death cannot always be prevented.16 20 More encouraging is the fact that cot deaths may already have become less frequent very recently in Britain, a judgment based on postneonatal mortality rates,21 22 the best available measure. During the 1960s, in sharp contrast to the previous two decades, the postneonatal mortality rate in England and Wales fell only slowly. In the '70s there has already been a 25°0 reduction, most of it since 1974. In Scotland the improvement has been even more striking: a 400, reduction between 1969 and 1976. This welcome trend is hard to explain at a time when the economic climate has been at its worst since the war. Future historians may point to NHS reorganisation, but contemporary observers would give them little support. Comparison with rates in other countries, however, indicates plenty of room for further improvement: the 1976 rates of 4.4/1000 live births for England and Wales23 and 4 5,/1000 live births for Scotland21 are still twice the Swedish rate23 of 2-2 in 1975. The DHSS multicentre study of postneonatal mortalitywith its painstaking, detailed clinical and pathological investigation of about 1000 deaths by 1979-should provide the first opportunity to assess the relative numerical importance of the different categories of cot death. There is real hope that this study will enable us to identify avoidable factors in the first category and aetiological leads for those cot deaths which are still difficult to explain. IWorking Party for Early Childhood Deaths in Newcastle, Archives of Disease in Childhood, 1977, 52, 828. 2 Cameron, J M, and Watson, E, 3ournal of Pathology, 1975, 117, 55. 3
4 5
6 7
8 9 1
McWeeny, P M, and Emery, J L, Archives of Disease in Childhood, 1975, 50, 191. Froggatt, P, Lynas, M A, and MacKenzie, G, British3'ournal of Preventive and Social Medicine, 1971, 25, 119. Prostestos, C D, et al, Archives of Disease in Childhood, 1973, 48, 835. Emery, J L, Swift, P G F, and Worthy, E, Archives of Disease in Childhood, 1974, 49, 686. Naeye, R L, et al, Journal of Pediatrics, 1976, 88, 511. Bergman, A B, and Wiesner, L A, Pediatrics, 1976, 58, 665. Naeye, R L, Ladis, B, and Drage, J S, American J'ournal of Diseases in Children, 1976, 130, 1207. Fleshman, J K, and Peterson, D R, American Journal of Epidemiology, 1977, 105, 555.
18 MARCH 1978
11 Carpenter, R G, and Emery, J L, Nature, 1977, 268, 724. 12 Carpenter, R G, et al, Archives of Disease in Childhood, 1977, 52, 606. Oakley, J R, Archives of Disease in Childhood, 1978, 53, 88. 14 Committee on Child Health Services (chairman Professor S D M Court), Fit for the Futuere. Lorndon, HMSO, 1976. 15 Cross, K W, and Lewis, S R, Archives of Disease in Childhood, 1971, 46, 13
211.
"( Steinschneider, A, Pediatrics, 1972, 50, 646. 17 Swift, P G F, and Emery, J L, Archives of Disease in Childhood, 1973, 48, 947. 18 Steinschneider, A, Pediatrics, 1975, 56, 967. 9 Nacye, R L, Archives of Pathology and Laboratory Medicine, 1977, 101, 165. 20 Shannon, D C, Kelly, D H, and O'Connell, K, Nezw England J7ournal of Medicine, 1977, 297, 747. 21 Registrar General for Scotland Annual Report, Part I. Edinburgh, HMSO, 1976. 22 Office of Population Censuses and Surveys, Series DH3, Number 2, Mortality Statistics: Childhood 1975. London, HMSO, 1977. 23 Office of Population Censuses and Surveys, unpublished information, 1978.
Mobility and the disabled Recent publications in that excellent series "Equipment for the Disabled" on outdoor transport' and wheelchairs2 have once again highlighted the problems of mobility, particularly for patients who are paraplegic or otherwise unable to walk. Since the Government bowed to the widely publicised campaign against the motorised three-wheeler these vehicles are no longer being supplied to the newly disabled. Indeed, the machine will be phased out of existence sooner or laterthough later may mean up to 20 years from now. Unfortunately, the mobility allowance-even with its recent increase-does not provide independence for all disabled people for whom a special vehicle would be appropriate. So we need to take a fresh look at the concept. Ideally two types of vehicle should be available. The premature withdrawal of the "Noddy" tricycle has left a need for a cheap, highly modifiable car-possibly something based on one of the hatchbacks. Most disabled people, however, need a safe, reliable, weatherproof, solo vehicle that is closer to a motorised wheelchair than a pseudocar. A battery-propelled all-weather chair would be stable, simple to control, and cheap-all features which should make it very appealing to the DHSS. Transport alone is not, however, enough. Architects, local authorities, and especially clerks of works should take note of the new edition3 of Selwyn Goldsmith's Designing for the Disabled. Mobility depends on access, and far too many of our public buildings and facilities are still not available to the disabled without (at times heroic) physical effort by them or their attendants. By now it should be possible to combine access for the disabled with aesthetic design without excessive
expenditure. Another neglected group are the elderly disabled, most of whom hardly use wheelchairs or powered transport. Many of them live at home, often effectively housebound because of unsuitability of public transport and lack of local shopping and other facilities. The primary problem may be difficulty in actually getting in and out of the house because of unsuitable steps and entrances. Stairs are difficult, if not impossible, for these patients; yet downstairs lavatories and bedrooms are exceptions in typical houses in industrial cities. The upstairs part is rarely used, and, while redundant, is often badly maintained. The elderly patients, mostly women, depend on neighbours and relatives for shopping, visiting, and social contact. Thirty years after the start of a comprehensive social welfare system surely these people's circumstances should be seen as
18 MARCH 1978
itself in the colon and then secrete an exotoxin with a necrotising effect on the colonic mucosa. Clearly the organism must be highly sensitive to vancomycin and non-absorbable sulphonamides. The new tools, then, in our management of pseudomembranous colitis are the screening test for toxin in the stools or in biopsy specimens; careful stool culture for pathogens; and the specific treatment with vancomycin. But we need to know whether other organisms and other toxins are concerned, and which antibiotics may be used to combat them. lDearing, W H, et al, Gastroenterology, 1954, 26, 38. 2Speare, G S, AmericantJouirnal of Suirgery, 1954, 88, 523. 3Bartlett, J G, and Gorbach, S L, Advances in Internal Medicine, 1977, 22, 455. 4Ecker, J A, et al, Amtiericani Yoturtnal of Gastroenterology, 1970, 54, 214. 5British Medical Journal, 1974, 4, 65. Miller, R R, and Hershel, J, Clinical Phlarnmacology anid Therapeutics, 1977, 22, 1. Tedesco, F J, et al, Annals of Inzternal Medicine, 1974, 81, 429. Buts, J P, et al, Gastroenterology, 1977, 73, 823. 9Price, A B, and Davies, D R, Youirnal of Clinical Pathology, 1977, 30, 1. Goodman, M J, and Truclove, S C, British Medical3Journal, 1976, 3, 354. L arson, H E, et al, British Medical Journal, 1977, 1, 1246. ' Rifkin, G D, et al, Lanicet, 1977, 2, 1103. 13 ILarson, H E, and Price, A B, Lancet, 1977, 2, 1312. " Small, J D, Laboratory Anlimal Care, 1968, 18, 411. 15 Bartlett. J G, ct al, Gastroenterology, 1977, 73, 772. "' Bartlett, J G, et al, Lancet, 1978, 1, 338.
Knowing the oxygenation of the fetus About half of all stillbirths are accounted for by infants who die, often during labour, with no discernible cause of death except "anoxia." While this diagnosis may be unhelpful as a basis for understanding primary causes, it has focused obstetricians' attention on a mode of death which should often be preventable. If during labour a fetus is known to be suffering lack of oxygen then rapid delivery and resuscitation may be lifesaving: indeed, these may save more than its life, since degrees of hypoxia which are not fatal seem likely to cause cerebral damage, and intellectual impairment of children may well be a much larger problem than perinatal death. The technological aspects of monitoring fetal wellbeing have evolved as part of the modern concept of intensive care applied to the fetuses of pregnant women thought to be at special risk. Nevertheless, the measurement of fetal oxygenation has proved technically elusive, and for the past 20 years the two most common approaches to the problem have been indirect. One has been to study fetal heart rate patterns, which are influenced by hypoxia, among other things; the other to study blood samples obtained from the fetal scalp, when acidosis (as indicated by the pH) has been the most used indicator of fetal hypoxia. While both techniques have made substantial contributions to perinatal care and fetal salvage, they have major shortcomings. The huge numbers of reports on fetal heart rate patterns have shown that they may change for many reasons apart from hypoxia,2 and the analysis and interpretation of these patterns are now considered so complex that resort has been made to computer analysis.3 Clearly, estimation of the pH in fetal scalp blood is a closer approach to fetal oxygenation, and some4 consider that abnormal fetal heart rate patterns are difficult to interpret without knowing the pH. But a fall in pH is a relatively late effect of hypoxia, and the intermittent
671
nature of blood sampling-a techi ique with its own hazardsmeans that hypoxia of rapid ons-L may not be detected in time. Ideally the obstetrician would like to have a direct and continuous record of fetal oxygen tension, and that ideal now seems to be within reach. The first supplement to be published by the British Journal of Obstetrics and Gynaecology5 presents the accumulated experience of a German and a Swedish team who have pioneered continuous transcutaneous monitoring of fetal oxygen tension in labour using a Clark type electrode fixed to the fetal scalp. Technical development of the electrode has resulted in one small enough to be applied through a cervix at least 3 cm dilated. It is fixed to the skin with a tissue glue, and an integral heater raises the temperature of the area below the electrode to 44°C for effective vasodilatation. Within 20 minutes a continuous record of Po, is available, and experience suggests that recordings for more than four hours are quite feasible. One of the most enlightening aspects of this report is the association between transcutaneous P02 levels and simultaneously recorded fetal heart rate patterns. The sinister implications of severe late decelerations were confirmed: in these circumstances the Po2 was always below 15 mm Hg, and similar Po, levels were associated with basal fetal heart rates of under 100 and over 180. Unexpectedly, loss of baseline variability of fetal heart rate was not always associated with a low P02. A further striking finding was the way in which supplementary oxygen given to the mother could raise the fetal Po0, and the way in which maternal apnoea after hyperventilation in labour could result in a dangerous fall in fetal P02. In transcutaneous monitoring perinatal medicine has a new and powerful tool, and both perinatal research and fetal clinical care should benefit. 1 Chamberlain, R, British Births, 1970, vol 1. London, Heinemann, 1975. 2 Ott, W J, Obstetrical and Gynecological Survey, 1976, 31, 339. Thomas, C, and Blackwell, R J, British J7ournal of Obstetrics and Gynaecology, 1975, 82, 634. 4 Beard, R W, Pediatrics, 1974, 53, 157. 5 Huch, A, et al, British J7ournal of Obstetrics and Gynaecology, 1977, 84, suppl 1.
What kind of cot death? Local studies of postneonatal mortality1 2 are gradually confirming the important point, made first by Sheffield researchers,3 that sudden unexpected deaths at home are a "mixed bag." We are beginning to recognise three categories: the baby whose acute infective illness is underestimated by health teams or parents and therefore does not receive the benefit of modern paediatric care; the baby who has an apparently minor illness which in some way triggers sudden death; and the baby who clinically and pathologically appears to have been well. This heterogeneity reduces the value of the epidemiological facts about cot death that continue to be gathered-age distribution, sex difference, seasonal variation, day of week and time of day found dead, mother's age, size of family, birth weight, length of gestation, complications of labour and delivery, method of feeding, mother's blood group, parental smoking, socioeconomic status of the family and of the geographical area, and the baby's level of activity and behaviour from birth.10 No study has attempted to differentiate its findings for the three clinicopathological categories of cot
BRITISH MEDICAL JOURNAL
672
death, usually because small numbers have made this impossible. Until this has been done, however, it is hard to see a logical application for the at-risk scoring concept proposed by the Sheffield group.11 12 A further problem with the Sheffield system is that in its existing form it does not seem to predict death as accurately in other cities.13 What, then, are the current prospects for preventing cot deaths ? For the first group-those who die from rapidly progressing and inadequately recognised infective illnessthere are clear preventive possibilities in improving the accessibility of health services for young children and in better training for doctors and nurses in recognising life-threatening paediatric conditions. Lasting progress seems more likely to come from organisational and training changes, embodying the spirit if not the letter of the Court proposals,14 than from specific measures directed at families with multiple "risk factors." If minor illnesses are important triggers of sudden death in the second group of cot deaths then improvements in general living conditions may be more important than health services. A large part of the explanation for the low incidence of cot death in countries such as Sweden may be related to housing, population density, and other special factors. Babies in the third group, who die without any observable illness, remain the most difficult problem. We have growing evidence that the mechanism of death may be apnoea similar to that seen in premature babies,15-20 but even on the rare occasions when it has been possible to identify babies at risk death cannot always be prevented.16 20 More encouraging is the fact that cot deaths may already have become less frequent very recently in Britain, a judgment based on postneonatal mortality rates,21 22 the best available measure. During the 1960s, in sharp contrast to the previous two decades, the postneonatal mortality rate in England and Wales fell only slowly. In the '70s there has already been a 25°0 reduction, most of it since 1974. In Scotland the improvement has been even more striking: a 400, reduction between 1969 and 1976. This welcome trend is hard to explain at a time when the economic climate has been at its worst since the war. Future historians may point to NHS reorganisation, but contemporary observers would give them little support. Comparison with rates in other countries, however, indicates plenty of room for further improvement: the 1976 rates of 4.4/1000 live births for England and Wales23 and 4 5,/1000 live births for Scotland21 are still twice the Swedish rate23 of 2-2 in 1975. The DHSS multicentre study of postneonatal mortalitywith its painstaking, detailed clinical and pathological investigation of about 1000 deaths by 1979-should provide the first opportunity to assess the relative numerical importance of the different categories of cot death. There is real hope that this study will enable us to identify avoidable factors in the first category and aetiological leads for those cot deaths which are still difficult to explain. IWorking Party for Early Childhood Deaths in Newcastle, Archives of Disease in Childhood, 1977, 52, 828. 2 Cameron, J M, and Watson, E, 3ournal of Pathology, 1975, 117, 55. 3
4 5
6 7
8 9 1
McWeeny, P M, and Emery, J L, Archives of Disease in Childhood, 1975, 50, 191. Froggatt, P, Lynas, M A, and MacKenzie, G, British3'ournal of Preventive and Social Medicine, 1971, 25, 119. Prostestos, C D, et al, Archives of Disease in Childhood, 1973, 48, 835. Emery, J L, Swift, P G F, and Worthy, E, Archives of Disease in Childhood, 1974, 49, 686. Naeye, R L, et al, Journal of Pediatrics, 1976, 88, 511. Bergman, A B, and Wiesner, L A, Pediatrics, 1976, 58, 665. Naeye, R L, Ladis, B, and Drage, J S, American J'ournal of Diseases in Children, 1976, 130, 1207. Fleshman, J K, and Peterson, D R, American Journal of Epidemiology, 1977, 105, 555.
18 MARCH 1978
11 Carpenter, R G, and Emery, J L, Nature, 1977, 268, 724. 12 Carpenter, R G, et al, Archives of Disease in Childhood, 1977, 52, 606. Oakley, J R, Archives of Disease in Childhood, 1978, 53, 88. 14 Committee on Child Health Services (chairman Professor S D M Court), Fit for the Futuere. Lorndon, HMSO, 1976. 15 Cross, K W, and Lewis, S R, Archives of Disease in Childhood, 1971, 46, 13
211.
"( Steinschneider, A, Pediatrics, 1972, 50, 646. 17 Swift, P G F, and Emery, J L, Archives of Disease in Childhood, 1973, 48, 947. 18 Steinschneider, A, Pediatrics, 1975, 56, 967. 9 Nacye, R L, Archives of Pathology and Laboratory Medicine, 1977, 101, 165. 20 Shannon, D C, Kelly, D H, and O'Connell, K, Nezw England J7ournal of Medicine, 1977, 297, 747. 21 Registrar General for Scotland Annual Report, Part I. Edinburgh, HMSO, 1976. 22 Office of Population Censuses and Surveys, Series DH3, Number 2, Mortality Statistics: Childhood 1975. London, HMSO, 1977. 23 Office of Population Censuses and Surveys, unpublished information, 1978.
Mobility and the disabled Recent publications in that excellent series "Equipment for the Disabled" on outdoor transport' and wheelchairs2 have once again highlighted the problems of mobility, particularly for patients who are paraplegic or otherwise unable to walk. Since the Government bowed to the widely publicised campaign against the motorised three-wheeler these vehicles are no longer being supplied to the newly disabled. Indeed, the machine will be phased out of existence sooner or laterthough later may mean up to 20 years from now. Unfortunately, the mobility allowance-even with its recent increase-does not provide independence for all disabled people for whom a special vehicle would be appropriate. So we need to take a fresh look at the concept. Ideally two types of vehicle should be available. The premature withdrawal of the "Noddy" tricycle has left a need for a cheap, highly modifiable car-possibly something based on one of the hatchbacks. Most disabled people, however, need a safe, reliable, weatherproof, solo vehicle that is closer to a motorised wheelchair than a pseudocar. A battery-propelled all-weather chair would be stable, simple to control, and cheap-all features which should make it very appealing to the DHSS. Transport alone is not, however, enough. Architects, local authorities, and especially clerks of works should take note of the new edition3 of Selwyn Goldsmith's Designing for the Disabled. Mobility depends on access, and far too many of our public buildings and facilities are still not available to the disabled without (at times heroic) physical effort by them or their attendants. By now it should be possible to combine access for the disabled with aesthetic design without excessive
expenditure. Another neglected group are the elderly disabled, most of whom hardly use wheelchairs or powered transport. Many of them live at home, often effectively housebound because of unsuitability of public transport and lack of local shopping and other facilities. The primary problem may be difficulty in actually getting in and out of the house because of unsuitable steps and entrances. Stairs are difficult, if not impossible, for these patients; yet downstairs lavatories and bedrooms are exceptions in typical houses in industrial cities. The upstairs part is rarely used, and, while redundant, is often badly maintained. The elderly patients, mostly women, depend on neighbours and relatives for shopping, visiting, and social contact. Thirty years after the start of a comprehensive social welfare system surely these people's circumstances should be seen as
