835LEADING ARTICLES

Separatism or Reintegration ?

THE LANCETLONDON 18 OCTOBER 1958

" THE need of these times ", we said six years ago,is to begin to reintegrate the various branches ofmedicine, and we do not believe that the best interestsof the profession will be served by separatist movementsthat may presently fill the medical scene with quite anumber of new colleges-not only of general practi-tioners, but also of pathologists, paediatricians, psychi-atrists, and others." The function of a college, as wesaw it, is something far bigger than to represent a groupof people who practise the same specialty: it is to pro-mote the growth of medical art and science over an areathat nowadays covers many specialties. We argued thatthe three Royal Colleges in London were in process ofbecoming colleges of medicine, surgery, and obstetrics,rather than closed corporations of physicians, surgeons,and obstetricians. We pointed to the developments thathave made the College of Surgeons the centre of a groupof affiliated faculties, and the College of Physicians " aremarkably catholic assembly, comprising almost everykind of doctor except (at present) general practitioners ".But appreciation of these fundamental changes, and oftheir implications, is still hindered by the fact that thesenior colleges have names given them in distant dayswhen there were only three specialties. Because inBritain the word " physician

" is now generally limitedto a particular kind of clinical consultant, the Collegeof Physicians is regarded by many outsiders as simplythe representative organ of this group. Indeed there aretimes when the college itself, hypnotised by its title,seems to take the same narrow view of its functions.Yet if it rejects its integrating role as a College ofMedicine, it will inevitably promote separatism, andthus reduce both its usefulness and its influence. Ifinternists claim a college of their own, they can scarcelyobject if each of the other vocational groups demands acollege too. (The contribution of some of them tomedicine is no less important than the internists’; andin twenty years’ time it may be more important.) Thatthe prestige of existing colleges must diminish witheach addition to their number may not matter if the

gains are proportionate; but we cannot think theywill be.

Each specialty, large or small, should have its voca-tional representative body-a faculty perhaps,2 or anassociation. But each specialty should also have accessto a college-an academic body of wider scope. In

pathology, allegiances and opinions have been divided;but Dr. McMENEMEY’s impressive presidential addressto the Association of Clinical Pathologists (p. 841) sounds

1. Lancet, 1952, i, 1392. ibid. 1951, ii, 1071.

like a final plea to the College of Physicians to givepathologists the academic home which there or else-where they must find. Not only does pathology stemfrom a clinical tradition but the pathologist of thefuture will remain, he believes, a doctor rather than atechnologist. Meanwhile, today, the pathologist’s clinicalresponsibility is high, and his " zeal for technical

efficiency ... should be no excuse for abandoning thatpostgraduate training in clinical medicine which allconsultants need to acquire ". Because a knowledge ofgeneral medicine is of more value to pathologists thanan acquaintance with anatomy or proficiency in sur-gical technique, their adherence " is primarily to theRoyal College of Physicians " : the pathologist is indeeda kind of physician. But all too often pathologists aredenied admission to the physicians’ college because theyhave been working more at the bench than at thebedside. An entrance examination with a pass-rate ofabout 12% is formidable to anybody, but in the presentmembership examination the emphasis is so stronglyclinical that few candidates can hope for success unlessthey have concentrated for some time on purely clinicalpractice. Hence its particular difficulty for pathologists." It is often in fact more than a difficulty, it is a deter-rent." Though young pathologists are commonlyrecommended to seek the membership, many refrainfrom doing so because the examination, as now arranged,is a disturbance to their education rather than an appro-priate part of it.

MCMENEMEY suggests that, without in any way lower-ing the high standard of its membership examination,the college should remove the disability it imposes onthe prospective pathologist-as might be done, perhaps,if rather lower marks in the clinical tests were accept-able from candidates who are prepared to demonstratetheir aptitude for pathology. Though to some clinicians(who properly set great store by the clinical exami-nation) this may seem a subversive proposal, we

hope they will refrain from dismissing it out of hand.An argument often put forward is that, since the

membership is a hallmark of clinical ability, its confer-ment on junior pathologists would cause confusion:indeed a pathologist might later secure a clinical post,improperly, on the strength of it. But this argument is

really no more than a relic from the days when theM.R.C.P. was regarded as a test of knowledge qualifyingits holder for work as a physician. In recent years the

college has repeatedly declared that the examination isnow, in fact, nothing of the kind: it is meant to be takentwo or three years after qualification and its purpose issimply to ascertain whether the candidate is qualified fortraining as a specialist-e.g., in a post as senior registrar.In Britain at least, consultant appointments are not madeon the strength of success in any examination (thoughsuch success may be one requirement), but mainlyon the doctor’s performance in his training post andafterwards; and it is inconceivable that anyone-werehe M.R.c.P. three times over-would be appointed as aclinical consultant unless he had also proved his clinicalability in many years of hospital practice. With only

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minor adjustment, the membership examination couldbe made an equally satisfactory test of the young doctor’ssuitability for training as a pathologist. If, having passedthis test, he afterwards changed his mind and took upclinical medicine, he would still have to demonstratehis clinical aptitude in competition with his clinicalcoevals. There would be no greater risk of erroneousselection for a consultant appointment than now existswhen a prospective clinician decides to make his careerin pathology.Remarking that in the past " many a physician has

been launched on a meteoric career from the ramp ofthe hospital laboratories ", MCMENEMEY says all too

truly that the National Health Service has facilitatedthe erection of barriers between the specialties. The

urgent desire of the colleges should surely be to breakdown such barriers, not to make them higher or morepermanent. For the Royal College of Physicians a

turning-point has been reached at which the choicebetween separatism and reintegration affects not onlypathologists but also its own future.

Crohn’s Disease after Twenty-five YearsNow that a quarter of a century has passed since

CROHN and his colleagues 1 first described terminalileitis (later known as regional ileitis, then regionalenteritis), what advances have been made? The

spectacular in medicine lies in the revelation of specificcure or of cause. With Crohn’s disease there has beenno such development; indeed the boundaries of itsclinical features have become blurred by terminologicaldifferences and even by uncertainty regarding its sitesof predilection. Though none would dispute that theterminal ileum is the commonest site of the gross lesions,other parts of the alimentary tract, from gullet to

anus, can be attacked. Dr. CROHN himself, after

reviewing his incomparable personal series of almost600 cases, considers that the large bowel is attacked

very rarely-probably in no more than 5% of cases-unless it has become involved secondarily from contactwith diseased ileum, by fistula formation, or afterresection.2 Yet in a British series reported by BROOKE 3the initial lesions were found to involve the large bowelin about half of 121 cases; and JACKSON 4 reports coloninvolvement in 31% of 126 cases treated at the Massa-chusetts General Hospital-though whether this involve-ment was primary is not stated. JACKSON also refersto a further 14 patients (making 43% in all) in whomulcerative colitis involved the whole colon at some timeafter regional enteritis was diagnosed. Unfortunately nospecific test, histological or biochemical, distinguishes theone from the other.

Ulcerative colitis proper affects primarily the largebowel, and any involvement of the small bowel usuallydevelops when the ileocxcal valve has become incom-petent and is insufficient to result in steatorrhaea

(which is present in many cases of Crohn’s ileitis).1. Crohn, B. B., Ginzburg, L., Oppenheimer, G. D. J. Amer. med. Ass.

1932, 99, 1323.2. Crohn, B. B. Address to British Society of Gastroenterology, November,

1957.3. Brooke, B. N. See Lancet, 1958, i, 1314.4. Jackson, B. B. Ann. Surg. 1958, 148, 81.

Furthermore, whereas in ulcerative colitis the gut wall isnot thickened, in Crohn’s disease it is considerably thick-ened. Fistula, other than anorectal, is extremely rare inulcerative colitis and usually develops because a pericolicabscess from a localised perforation has burst throughinto an adjacent viscus (stomach or jejunum, for

example); whereas in Crohn’s disease fistula formationis fairly common but does not appear to result fromsuch acute crises (perforation is rare 5), but instead

develops gradually from contact with the inflamedintestine. In ulcerative colitis the mucosa between ulcersseldom appears normal, though it often remains so

proximal to ulcers in the transverse or descending colon;in Crohn’s disease ulcers in the colon appear more dis-crete because of the apparent normality of the inter-vening mucosa. Differentiation of the two disorders is

important not only for a better understanding of thembut also because surgical techniques for ulcerative colitismay be unsuitable for Crohn’s disease. In Crohn’sdisease small-bowel lesions have developed above anileostomy after proctocolectomy 6; and one of JACKSON’S14 patients with the " combined " disease died from

ileostomy dysfunction. 7 YARNIS et awl. have drawnattention to the difficulty in treating combined forms.The chief advances in Crohn’s disease have followed

painstaking study of series of cases over years. CROHNhas observed that we shall not have a full picture untilthe disease has been studied throughout a life’s span.It commonly affects adolescents, and most patients areexpected to live their normal span ;5 so a fair prognosismay be given, though the patient will undoubtedly haveto endure corticoids, surgery, and periods of incapacityon the way. Only 85 of 542 patients in CROHN’s seriesescaped operation, and of these the disease was con-sidered to be arrested in 51.5 Here is an odd paradox:that 80% have been submitted to operation, thoughsurgery is no longer the treatment of choice. The passingof the anatomical era in surgery has damped the desireto cut any abnormality out as soon as it is detected; withregional enteritis the itching fingers are learning to

withhold. Surgical minds are now alive to the possi-bility that invisible defects lie apart from the grosslesion-lurking there to cause overt recurrence anotherday.As follow-up studies have been extended to ten and

even fifteen years so recurrence-rates of 60-80% havebeen reported.9 9 Extrapolation of these figures wouldsurely give a 100% recurrence-rate in a normal life-span;yet the recent statistics from CROHN show that the ratewas 27% in a follow-up period extending from one totwenty-five years.5 JACKSON, who reports an overallrecurrence-rate of 55% and spontaneous remission inonly just over 1% in a follow-up of 126 cases over twoto twenty years, considers that, despite many examplesof recurrence fifteen to twenty years later, a patient who5. Crohn, B. B. Gastroenterologia, 1958, 89, 352.6. Brooke, B. N. Ann. R. Coll. Surg. Engl. 1957, 20, 114.7. Jackson, B. B. Ann. Surg. 1958, 148, 88.8. Yarnis, H., Marshak, R. H., Crohn, B. B. J. Amer. med. Ass. 1957,

164, 7.9. Van Patter, W. N., Bargen, J. A., Dockerty, M. B., Feldman, W H,

Mayo, C. W., Waugh, J. M. Gastroenterology, 1954, 26, 347. Cooke,W. T. Ann. R. Coll. Surg. Engl. 1955, 17, 137.

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has been free of trouble for over four years is likely toremain so. Nevertheless the high rate of recurrence hascaused surgeons to abandon attempts at cure and

instead to concentrate on " holding " operations-

operations to keep the patient going. Accordingly, at theoutset remission is obtained by conservative means-notably administration of corticosteroids and vitamin B12and remedying of potassium loss-and operation is

withheld until obstruction, fistula, or intractablediarrhoea demand intervention.

Opinion differs regarding the surgical method, forthough at Mount Sinai Hospital CROHN opts for bypassby anastomosis and exclusion, since the recurrence-rateis no greater than that following resection while theoperative mortality is half (4% compared with 9- 6%),selsewhere resection is preferred 10; and at Boston 4 theoperative mortality figures are reversed (7% in 57 short-circuit operations, compared with 4.5% in 86 resections),though the effect of reserving short-circuit for the moredifficult case must here be borne in mind. Perhaps aftera quarter of a century, though we know the diseasebetter, we understand it less. -

10. See Lancet, 1958, i, 1315.11. Smith, H. V., Daniel, P. Tubercle, Lond. 1947, 28, 64.12. Lorber, J. Amer. Rev. Tuberc. 1958, 78, 38.13. Acheson, R. M., Smith, H. V. Quart. J. Med. 1958, 27, 83.

Long-term Outcome in TuberculousMeningitis

IT is now eleven years since streptomycin was firstused for the treatment of tuberculous meningitis.Much attention has been given to the use of this drugalone and in conjunction with others, such as isoniazid,p-aminosalicylic acid, the corticosteroids, and intra-

thecal tuberculoprotein. Growing emphasis has beenplaced on diagnosis and proper treatment early in thedisease: the tuberculous process has an aptitude forproducing both endarteritis and constrictive exudatesround that most eloquent part of the central nervoussystem, the midbrain," and it is essential to arrest its

progress before function is irreversibly impaired.Nowadays a two-year survival-rate of less than

80% suggests that the treatment was at fault, and ofthe survivors very few should have residual disabilityother than loss of vestibular function. But what of the

long-term follow-up ? There are no really adequatepublished accounts from any of the recognised treat-ment centres, although recent papers 12 13 have givenimportant information in a condensed form. There arethree broad considerations here: (1) the effects ofirreversible neurological damage sustained during theacute illness; (2) the incidence of late relapse; and3) the delayed onset of disorders produced either

by organisation of or by enlargement of residualtuberculous lesions.

Irreversible damage is generally agreed to arise mostcommonly in patients in whom the disease is advancedat the start of treatment. Hemiplegia, optic atrophy,and dementia are almost certainly due to the diseaseitself; whereas deafness and cauda-equina lesions (thelatter fortunately rare) are probably iatrogenic, the

former being due to streptomycin and the latter to

traumatic spinal puncture. Published accounts are

most heartening in suggesting that even severe disabilityhas not prevented full-time employment of treated

adults, and that the majority of children do not subse-quently show much mental or physical disability.Publication of detailed studies of these points wouldbe welcome.

By analogy with tuberculous disease in other organs,foci of viable organisms might survive in a quiescentstate for many years before giving rise once more toactive, widespread disease. The reported incidence ofsuch late relapses-as opposed to those within monthsafter treatment has been stopped-is surprisingly low.In the Oxford series 14 no patient among those treatedthere from the outset has relapsed after treatment andfull convalescence; and LORBER 12 15 reports only 7 clear-cut relapses between one and eight years after the firstattack. Delayed neurological and endocrinologicalcomplications are also rare. Focal epilepsy 16 anddiabetes insipidus and sexual disturbances 15 have beenreported. The infrequency of the last two is surprising inview of the propensity of the tuberculous process forforming exudate in the basal cisterns and round thebrain-stem. It is also remarkable that cord lesions areso infrequent. The high incidence of paraplegia reportedby BROOKS et al. 17 is unusual, although postmortemexamination of the spinal cord after death at the heightof the illness shows an astonishing amount of exudate inthe meninges compressing the cord, especially when aspinal block is present.

In contrast to the low incidence of relapse and otherlate complications is the high incidence of intracranialcalcification after treatment, reported notably byLORBER 12 18 and ACHESON and SMITH 13 in their radio-

graphic studies. LoRBER showed that in 68% of childrendetectable calcification had developed two and a halfyears or more after treatment; and the findings ofAcHESON and SMITH essentially agree with his. Calcifica-tion is commoner in children than adults, and in

patients whose treatment was not started until thedisease was advanced. It is commonest in the basal

meninges and may thus be correlated with the mostimportant site of exudate in the active infection. Theincidence is a little higher in patients with neurologicalsequelae than in others. Both LoRBER and the Oxfordworkers have investigated radiographically an impressiongained from postmortem study that intrathecal tuber-culin helps to resolve tuberculous exudate. Theirobservations on intracranial calcification suggest thatthis impression is correct; but the numbers were

insufficient for a firm conclusion. It seems that only along-term follow-up will show whether there is anyrelation between the exact form of treatment, theincidence of intracranial calcification, and the ultimateprognosis.14. Smith, H. V., Vollum, R. L., Taylor, L. M., Taylor, K. B. Tubercle,

Lond. 1956, 37, 301.15. Lorber, J. Arch. Dis. Childh. 1958, 33, 315.16. Lorber, J. Proc. R. Soc. Med. 1951, 44, 916.17. Brooks, W. D. W., Fletcher, A. P., Wilson, R. R. Quart. J. Med. 1954,

23, 275.18. Lorber, J. Arch. Dis. Childh. 1952, 27, 542.