136 this the curriculum for the diploma of public health is partly responsible. So little attempt does it make to orient the future medical officer of health to this .aspect of his duties that he is often less well informed .about mental health than a recently trained health visitor. Indeed, a British nurse engaged in public- health work, who attended one of the W.H.O. seminars on the subject, remarked ruefully that she did not know how she was going to get the mental- health point of view across to the doctor under whom she was working. In saying this we do not, of course, imply that the training of health visitors in mental health is by any means perfect : both their training and that of the future medical officers of health requires revision and reorientation if this work is to be done ; and courses are also badly needed for those already engaged in this field. Proposals for such instruction regularly encounter opposition from those who have matured in another tradition : " what," these are inclined to ask, " can anyone tell us about the management of mental-health problems which we .are not already doing on common-sense grounds ? " But it is also usual, as a course proceeds, for this resistance to melt : the very common-sense of the participants leads them to accept the new approaches opened up for them. Nevertheless, as Prof. G. KRAUS 3 has suggested, where resistance is strong it may be wise to begin by training a few people only-choosing those least at odds with the notions of psychiatry- and leaving them for a time to leaven the lump of their co-workers. " What is there to teach, anyway ? " is another frequent question, and a far-reaching one ; and the tentative suggestions of the L.C.C. study group hardly begin to touch on the answer. Of course the first months and years of life are important ; of course the mother can do much in those years to make or mar the emotional development of her child and his subsequent mental health; and of course the maternity and child-welfare centres should accept the responsibility for teaching her what to do and-equally important—what not to do. But the causes of mental ill health do not all begin to operate at the birth of the child : some begin much earlier. Dr. G. R. HARGREAVES,8 whose paper we published recently, shares CAPLAN’S view that mental-health teaching should begin in the antenatal clinic, in time to allay the fears and anxieties of the mother during her pregnancy. Such fears, when disregarded, some- times end in psychosis or severe neurosis which may demand months or years of treatment. At an earlier stage, HARGREAVES says, the symptoms are still plastic, and simple measures may tip the balance towards adjustment and recovery. Many fears of the pregnant woman are absurd and archaic, but they are none the less alarming on that account: it does no good, and may do harm, to pooh-pooh them. llany of her anxieties, on the other hand, are well grounded, centring on the change in human relations which the birth of a baby brings to every family. Quite simple teaching at the antenatal clinic, as well as group discussions of the kind suggested by CAPLAN, can help the mother at this time ; and even the obstetrician, as HARGREAVES suggests, should be able to give such help, and be willing when necessary to seek the collaboration’ of a psychiatrist in bringing the mother, whole and safe, through pregnancy, 8. Ibid, Jan. 1, 1955, p. 39. labour, and the puerperium. Indeed, QUERIDO holds that the duty of the public-health service to prevent mental ill health runs throughout the lives of even- one of us, and should properly embrace mothers. infants, preschool and school children, young people at work, university students, those in their working years, women at the menopause, and the aged, as well as those whose mental well-being is assailed by special hazards-such as patients discharged from men. tal hospitals, people living in overcrowded slums, unmarried mothers, those discharged from prisons, young delinquents, the disabled, and those suffering from diseases (such as tuberculosis and venereal disease) which affect their lives in the community. Much of the work done by our public services already has some bearing on the mental health of many of these people : the children’s officers, the psychiatric social workers, and the probation officers are all aware of this side of their efforts. What is now needed is to make what is implicit outspoken, and to extend the principles of mental hygiene into every part of public-health work. It is an urgent task : not only our slums but our mental hospitals are overcrowded, and more of us are nowadays hampered by neurosis and other forms of mental ill health than by the diseases which sprang from lack of sanitation. Our sickness has changed, and public needs rather than tradition should now dictate the pattern of our public-health service. 1. von Euler, U. S., Liljestrand, G. Acta. physiol. scand. 1946 12, 301. 2. Motley, H. L., Cournand, A., Werkö, L., Himmelstein, A. Dresdale, D. Amer. J. Physiol. 1947, 150, 315. Pulmonary Hypertension PULMONARY hypertension is now a well-recognised disorder, but much remains to be discovered about its aetiology. Usually it is a complication of cardiac or pulmonary disease, but occasionally it is found in the absence of either. The normal pulmonary vascular resistance is low, and the pulmonary-artery pressure is less than the systemic, even in the presence of con- siderable variations in pulmonary blood-flow. Pulmo- nary hypertension can result either from a greatly increased pulmonary blood-flow (such as occurs with a large patent ductus arteriosus) or from an increase in the pulmonary vascular resistance. Sometimes more than one mechanism operates in the same patient, as in patent ductus arteriosus with narrowing of the pulmonary arterioles. In mitral stenosis hyper- tension in the lesser circulation may result either from an increase in pulmonary venous pressure caused by the increased resistance at the mitral valve, or from an increase in arteriolar resistance. Severe pulmonary- arterial hypertension is always due to reduction in the pulmonary vascular bed at the pre-capillary or arteriolar level. The causes of this reduction may be obstructive (as in repeated pulmonary embolism. various forms of pulmonary arteritis, or carcinomatosis) or secondary to pulmonary fibrosis or emphysema. Problems in the elucidation of pulmonary hyper- tension centre mainly around the mechanism respon- sible for reduction in the lumen of the arterioles, and for the organic changes which may also be present. It has been known for some years that acute hypoxia can cause pulmonary vasoconstriction and a rise in pulmonary-artery pressure.1 2 This mechanism may
Transcript
136
this the curriculum for the diploma of public healthis partly responsible. So little attempt does it maketo orient the future medical officer of health to this
.aspect of his duties that he is often less well informed
.about mental health than a recently trained healthvisitor. Indeed, a British nurse engaged in public-health work, who attended one of the W.H.O.seminars on the subject, remarked ruefully that shedid not know how she was going to get the mental-health point of view across to the doctor under whomshe was working. In saying this we do not, of course,imply that the training of health visitors in mentalhealth is by any means perfect : both their trainingand that of the future medical officers of health
requires revision and reorientation if this work is tobe done ; and courses are also badly needed for thosealready engaged in this field. Proposals for suchinstruction regularly encounter opposition from thosewho have matured in another tradition : " what,"these are inclined to ask, " can anyone tell us aboutthe management of mental-health problems which we.are not already doing on common-sense grounds ?
"
But it is also usual, as a course proceeds, for thisresistance to melt : the very common-sense of the
participants leads them to accept the new approachesopened up for them. Nevertheless, as Prof. G. KRAUS 3has suggested, where resistance is strong it may bewise to begin by training a few people only-choosingthose least at odds with the notions of psychiatry-and leaving them for a time to leaven the lump of theirco-workers.
" What is there to teach, anyway ? " is another
frequent question, and a far-reaching one ; and thetentative suggestions of the L.C.C. study group hardlybegin to touch on the answer. Of course the firstmonths and years of life are important ; of coursethe mother can do much in those years to make ormar the emotional development of her child and hissubsequent mental health; and of course the
maternity and child-welfare centres should accept theresponsibility for teaching her what to do and-equallyimportant—what not to do. But the causes ofmental ill health do not all begin to operate at thebirth of the child : some begin much earlier. Dr. G. R.HARGREAVES,8 whose paper we published recently,shares CAPLAN’S view that mental-health teachingshould begin in the antenatal clinic, in time to
allay the fears and anxieties of the mother duringher pregnancy. Such fears, when disregarded, some-times end in psychosis or severe neurosis which maydemand months or years of treatment. At an earlierstage, HARGREAVES says, the symptoms are still
plastic, and simple measures may tip the balancetowards adjustment and recovery. Many fears of thepregnant woman are absurd and archaic, but theyare none the less alarming on that account: it doesno good, and may do harm, to pooh-pooh them.llany of her anxieties, on the other hand, are wellgrounded, centring on the change in human relationswhich the birth of a baby brings to every family.Quite simple teaching at the antenatal clinic, as wellas group discussions of the kind suggested by CAPLAN,can help the mother at this time ; and even theobstetrician, as HARGREAVES suggests, should be ableto give such help, and be willing when necessary toseek the collaboration’ of a psychiatrist in bringingthe mother, whole and safe, through pregnancy,
8. Ibid, Jan. 1, 1955, p. 39.
labour, and the puerperium. Indeed, QUERIDO holdsthat the duty of the public-health service to preventmental ill health runs throughout the lives of even-one of us, and should properly embrace mothers.infants, preschool and school children, young people atwork, university students, those in their working years,women at the menopause, and the aged, as well asthose whose mental well-being is assailed by specialhazards-such as patients discharged from men.
tal hospitals, people living in overcrowded slums,unmarried mothers, those discharged from prisons,young delinquents, the disabled, and those sufferingfrom diseases (such as tuberculosis and venerealdisease) which affect their lives in the community.Much of the work done by our public servicesalready has some bearing on the mental health of
many of these people : the children’s officers, the
psychiatric social workers, and the probation officersare all aware of this side of their efforts. What isnow needed is to make what is implicit outspoken,and to extend the principles of mental hygiene intoevery part of public-health work. It is an urgenttask : not only our slums but our mental hospitalsare overcrowded, and more of us are nowadayshampered by neurosis and other forms of mentalill health than by the diseases which sprang fromlack of sanitation. Our sickness has changed, andpublic needs rather than tradition should now dictatethe pattern of our public-health service.
1. von Euler, U. S., Liljestrand, G. Acta. physiol. scand. 194612, 301.
2. Motley, H. L., Cournand, A., Werkö, L., Himmelstein, A.
Dresdale, D. Amer. J. Physiol. 1947, 150, 315.
Pulmonary HypertensionPULMONARY hypertension is now a well-recognised
disorder, but much remains to be discovered about itsaetiology. Usually it is a complication of cardiac orpulmonary disease, but occasionally it is found in theabsence of either. The normal pulmonary vascularresistance is low, and the pulmonary-artery pressureis less than the systemic, even in the presence of con-siderable variations in pulmonary blood-flow. Pulmo-nary hypertension can result either from a greatlyincreased pulmonary blood-flow (such as occurs witha large patent ductus arteriosus) or from an increasein the pulmonary vascular resistance. Sometimesmore than one mechanism operates in the same
patient, as in patent ductus arteriosus with narrowingof the pulmonary arterioles. In mitral stenosis hyper-tension in the lesser circulation may result either froman increase in pulmonary venous pressure caused bythe increased resistance at the mitral valve, or from anincrease in arteriolar resistance. Severe pulmonary-arterial hypertension is always due to reduction inthe pulmonary vascular bed at the pre-capillary or
arteriolar level. The causes of this reduction maybe obstructive (as in repeated pulmonary embolism.various forms of pulmonary arteritis, or carcinomatosis)or secondary to pulmonary fibrosis or emphysema.
Problems in the elucidation of pulmonary hyper-tension centre mainly around the mechanism respon-sible for reduction in the lumen of the arterioles, andfor the organic changes which may also be present.It has been known for some years that acute hypoxiacan cause pulmonary vasoconstriction and a rise in
pulmonary-artery pressure.1 2 This mechanism may
137
be important in patients with pulmonary heart-disease. in whom the pulmonary-artery pressure risesconcomitantly with a fall in arterial oxygen saturationduring an acute respiratory infection, althoughrestoration of the arterial saturation to normal is not
always followed by a fall in the pulmonary-arterypressure.3 In pulmonary fibrosis and in emphysema,diminished elasticity of the lungs and destruction ofthe small blood-vessels reduces the vascular bed andincreases the resistance ; uneven ventilation causesanoxia, and tends to perpetuate a vicious circle whichends in established pulmonary hypertension and rightventricular failure. In addition to hypoxia, drugs- uch as noradrenaline may cause arteriolar constric-tion.4 while tolazoline hydrochloride (’ Priscol’) hasbeen said to lower the pulmonary vascular resistancein primary pulmonary hypertension. 5 GrLMOREet al. 6have suggested that the pulmonary vessels in man areunder autonomic control, but this view has been
challenged by LEE et al. 7 Heart-disease accompaniedby an increase in arteriolar resistance may be con-genital or acquired. Organic changes in the arteriolesleading to reduction in their lumen are common inpatent ductus arteriosus and in ventricular septaldefect, but less so in atrial septal defect.8 EvANs 9has demonstrated arteriolar endarteritis in suchcases, and on injection of the lungs post mortemhas found " pruning
" of the terminal branches of the
pulmonary tree. Arteriosclerotic and other organicarteriolar changes have also been shown by otherworkers.10 11 The cause of such changes is unknown.CIVIN and EDWARDS 12 13 have found that the foetal
type of pulmonary arteriole (in which the lumen of thevessel is less than the transverse diameter of thevessel wall) may be present in the Eisenmengersyndrome, and have suggested that the high arteriolarresistance so produced constitutes a protective mecha-nism which prevents the lungs from being flooded withblood under high pressure in this and other congenitaldisorders. In patent ductus arteriosus the pulmonary-artery pressure may become so high that the shuntreverses, or may cease entirely.
In the realm of acquired heart-disease, mitralstenosis is one of the most usual causes of pulmonaryhypertension. Increased arteriolar resistance iscommon, and has been shown to be due both toorganic narrowing 14 15 and to reversible or functionalnarrowing.16 17 Narrowing is not confined to thearterioles; it has been shown by angiocardiographyto occur in the small muscular arteries.18 The cause
3. Mounsey, J. P. D.. Ritzmann, L. W., Selverstone, N. J., Briscoe,W. A., McLemore, G. A. Brit. Heart J. 1952, 14, 153.
4. Besterman, E. M. M. Brit. med. J. 1951, ii, 205.5. Dresdale, D. T., Schultz, M., Michtom, R. J. Amer. J. Med.
1951, 11, 686.6. Gilmore, H. R., Kopelman, H., McMichael, J., Milne, I. G.
Lancet, 1952, ii, 898.7. Lee, G. de J., Matthews, M. B., Sharpey-Schafer, E. P. Brit.
Heart J. 1954, 16, 233.8. Swan, H. J. C., Zapata-Diaz, J., Burchell, H. B., Wood, E. H.
Amer. J. Med. 1954, 16, 12.9. Evans. W. Proc. R. Soc. Med. 1951, 44, 600.10. Welch, K. J., Kinney, T. D. Amer. J. Path. 1948, 24, 729.11. Old. J. W., Russell, W. O. Ibid, 1950, 26, 789.12. vin. W. H., Edwards, J. E. Circulation, 1950, 2, 545.13. IVIN. W H., Edwards, J. E. Arch. Path. (Lab. Med.) 1951,51, 192.14. Parker, F., Weiss, S. Amer. J. Path. 1936, 12, 573.15. Larrabee, W. F., Parker, R. L., Edwards, J. E. Proc. Mayo
Clin. 1949, 24, 316.16. Bayliss, R. I. S., Etheridge, M. J., Hyman, A. L. Lancet,
1950, ii, 889.17. Lewis, B. M., Gorlin, R., Houssay, H. E. J., Haynes, F. W.,
Dexter, L. Amer. Heart J. 1952, 43, 2.18. Davies, L. G., Goodwin, J. F., Steiner, R. E., Van Leuven,
B. D. Brit. Heart J. 1953, 15, 393.
of this arterial and arteriolar narrowing is unknown ;possibly it is induced in some way by the elevatedleft-auricular and pulmonary-capillary pressures.Anoxia may be a factor, since oxygen inhalation hasbeen shown to lower the resistance.19 WOOD 20 hasfound that in mitral stenosis with a very high pul-monary vascular resistance there is right ventricularinsufficiency rather than pulmonary congestion.Arteriolar constriction is now usually regarded as aprotective mechanism which shields the pulmonarycapillaries from the powerfully acting right ven-
tricle 17 21 ; but this view has been challenged byDAVIES et al.22 These workers have shown that inmitral stenosis the total pulmonary vascular resistancecan be reduced by hexamethonium bromide withoutproducing pulmonary congestion or oedema ; and theyclaim that attacks of pulmonary oedema are commonerin patients with an increased vascular resistance thanin those without. Unfortunately their data are notsufficiently complete to show conclusively that hexa-methonium acts solely by dilating the pulmonaryblood-vessels through a reduction in arteriolarresistance ; reduction in systemic as well as pul-monary resistance may play a part.23 While it seems
likely that an extreme arteriolar resistance shields thepulmonary capillaries at the expense of the rightventricle, this may not always prevent pulmonaryoedema, nor is it necessarily beneficial.In recent years there have been many reports of
pulmonary hypertension due to an increased arteriolarresistance in the absence of congenital or acquiredheart-disease or of pulmonary disease. In 1940DE NAVASQUEZ et al.24 described cases of rightventricular hypertrophy of unknown aetiology inwhich the pulmonary arterioles were normal at
necropsy. DRESDALE et a1.5 in 1951 reviewed"
primary " or " essential " pulmonary hypertension,
which predominantly affects young people, and ischaracterised by symptoms and signs of severe
pulmonary hypertension due to a high arteriolarresistance, without any cardiac or other pulmonarydisease. WOOD 21 drew attention to the occurrencein this disorder of tiredness, dyspnoea, syncope, andeven angina of effort, and of a small pulse and coldextremities, a giant " a
" wave in the jugular venous
pulse, right ventricular hypertrophy, narrow duplica-tion of the second heart-sound with accentuation ofthe pulmonary element, and sometimes pulmonarysystolic or diastolic murmurs. Cardioscopy showsenlargement of the right auricle, ventricle, and pul-monary artery, with clear peripheral lung fields. The
electrocardiogram shows distinct right ventriculardominance. The arterial-oxygen saturation is initiallynormal but may become slightly reduced as the diseaseprogresses ; yet cyanosis, when present, is usuallyperipheral. Recently CUTLER et al.25 have describedseven patients with this disorder, which they havedesignated the pulmonary vascular obstruction syn-19. McGregor, M., Bothwell, T. H., Zion, M. M., Bradlow, B. A.
Amer. Heart J. 1953, 46, 187.20. Wood, P. Brit. med. J. 1954, i, 1051, 1113.21. Wood, P. Brit. med. Bull. 1952, 8, 348.22. Davies, L. G.. Goodwin, J. F., Van Leuven, B. D. Brit. Heart J.
1954, 16, 440. 23. Storstein, O., Tveten, H. Scand. J. clin. Lab. Invest. 1954,
6, 169.24. De Navasquez, S., Forbes, J. R., Holling, H. E. Brit. Heart J.
1940, 2, 177.25. Cutler, J. G., Nadas, A. S., Goodale, W. T., Hickler, R. B.,
Rudolph, A. M. Amer. J. Med. 1954, 17, 485.
138
drome. All -had extremely high pulmonary arteriolarresistances, and at necropsy in two of the cases thepulmonary arterial tree showed patchy atheroma, thelarge elastic branches having hyperplasia of the mediawith duplication of the elastic lamina and slightdegenerative changes. The muscular pulmonaryarteries were the seat of pronounced subendothelialfibrosis, often occluding the lumen ; many wereobliterated by -thrombi. The capillaries and veinswere normal. GILMOUR and EVANS26 describedendarteritis fibrosa in the muscular pulmonary arteriesin a case of primary pulmonary hypertension, andconcluded that these changes might be secondary tothe hypertension. Necropsy studies in other series 24have not always revealed anv definite vascular
abnormality ; and DRESDALE et al. 5 considered thatthe anatomical changes present in some cases mightbe secondary to neurogenic vasoconstriction. Cor pul-monale due to multiple pulmonary emboli has beendescribed,27 but CUTLER et al.25 do not regard thisas the cause in their cases. They suggest that anextremely high arteriolar resistance in congenitalheart-disease (particularly ventricular septal defect)may be due to a separate, possibly genetically deter-mined, pulmonary vascular disorder. WOOD 21 empha-sises the rapid progression of primary pulmonaryhypertension, but the condition of two of the patientsdescribed by CUTLER et al. did not deteriorate for
twenty to thirty years. They mention the risk in suchcases of sudden death, and remark that these
patients tolerate any diagnostic procedure badly ;one of their patients died suddenly during cardiaccatheterisation.The organic arteriolar changes found in severe
pulmonary hypertension, from any cause, havefeatures in common; the factors responsible forarteriolar constriction may also be similar. Until thismechanism is known much will remain obscure, butstudies with drugs which cause arteriolar dilatationmay yield further important information. Furtherexamination of the bronchial circulation may alsothrow light on disordered function of the pulmonaryvascular system.211 Meanwhile it is useful to rememberthat the clinical picture of severe pulmonary hyper-tension is remarkably constant, whatever the cause,and resembles that of the " essential " type, especiallyin patent ductus arteriosus where the flow may bereversed and the typical murmur absent, and inmitral stenosis where the diagnostic auscultatory signsmay be negligible or absent as a result of the greatlyreduced flow through the mitral valve. Treatment ofthe pulmonary vascular obstruction syndrome is
unsatisfactory, except in mitral stenosis where success-ful valvotomy may be followed by a fall in vascularresistance,29 and in patients with a patent ductuswhich has been ligated before the shunt has ceasedor reversed. Accurate diagnosis, which is oftenpossible only by cardiac catheterisation or angio-cardiography. is therefore essential. For the rest,treatment with vasodilator drugs, such as tolazolineor methonium compounds, 5 21 22 may be worth trying.26. Gilmour, J. R., Evans, W. J. Path. Bact. 1946, 58, 687.27. Owen. W. R.; Thomas. W. A., Castleman, B., Bland, E. F.
New Engl. J. Med. 1953, 249, 919.28. Marchand, P., Gilroy, J. C., Wilson, V. H. Thorax, 1950,
The Fertility of British WomenTHE fears so often expressed about the agein-2
of our population and the decline of our birth-rat’-led to the appointment of a Royal Commission onPopulation whose final paper, on the trend and
pattern of fertility in Great Britain, appeared latweek. 2 Though ’’ planning
’’ is a word which lia,lost a little of its pristine savour, some intelligentpredictions must be made about the results of presenttrends in fertility and family size if our difficultiesare to be anticipated and resolved. To obtain th-basic data, the commission asked Prof. D.’V. GLASSand Prof. E. GREBENIK to undertake a family censusencompassing more than a million women in theUnited Kingdom. Their report on this census
conducted in 1946, has interest as much for thediscussion of methods as for the results.
This survey, supported by none of the legal sanctionsof a national census, relied entirely on the cooperationof individual women ; public relations were thereforevital. Press and B.B.C. publicity was considerableand in the main helpful, though some papers railedagainst " snooping " which was " entirely repugnantto the British sanctity of the home which has hithertobeen our national heritage." On the day, everytenth reference leaf was drawn from the alphabeticalration-book file at every food office in Great Britain.From that sheet the names of all apparently marriedor widowed women were extracted, and questionarieswere despatched to them by post. These women.
’ who formed a representative 10% sample of thenational total, were asked to report their marital
status, the number and dates of birth of their children.and their husband’s occupation. Thirteen thousand
locally recruited enumerators called on them laterto collect and check on their replies. In all sampleinquiries a high response ratio is essential to success:and for a voluntary inquiry of this type, the 87.5%reply was remarkable. A personal letter from thechairman of the commission, emphasising the import-ance and confidentiality of the inquiry, produceda response from some of the more reluctant. Nocontact could be made with women who existed onlyin the imagination of those who profited by theirration books, while in some sections of London therewas little hope of finding women " at home ’’ at anaccommodation address, even in the required threecalls. In the second week of the census coincidentalannouncement in the House of Commons of theend of the supply of dried eggs and the cost of thefamily census stirred up adverse comment, and thicaused a sharp acceleration in the usual increase in thenon-response rate which comes with deepening apathyand resistance. Response-rates differed accordingto the region of the country ; surprisingly, theNortherners proved particularly docile, while theworst response-rates were in the larger urban area-where problems of contact were greatest. Coopera-tion depended, above all, on the interviewer, who didbest when he combined previous experience with
subtlety of approach-as in the enumerator who
1. Report of the Royal Commission on Population H.M StationeryOffice. 1949. See Lancet, 1949, i, 1105, 1110.
2. The Trend and Pattern of Fertility in Great Britain: A Reporton the Family Census of 1946, by D. V. GLASS and E. GREBENTHPart 1 : Report. Part 2 : Tables. H.M. Stationery Office1955. Pp. 306 and 253. 70s. the pair.
