PSYCHIATRY AND HOSPITAL ADMINISTRATION

150

phasic lesions are allowed to begin the more certain it is that by middle age the end stages will be reached. Surgeons and anaesthetists must accept that even distinguished physicians with the full backing of their hospital aids are unable on many occasions to diagnose the presence of advanced coronary disease. A man aged 41 years was actually sent to a mental hospital although he had enormous myocardial scars; this was because for several years all the clinical tests, including E.C.G., showed his heart

to

be normal. What chance have

we

with

a man

aged 35 years who prided himself on his physical fitness as boxer and swimmer until 13 hours before his death from an hour after admission to hospital ? The medical profession will find little but humiliation in our present practice with coronary disease. I often find it much more difficult to explain why a patient has lived a more or less normal life for so long with his coronary disease than why he has died from it. The reasons for this seem to be: a

coronary disease

(1) The physiological reserve in the coronary supply must be enormous, at least 7 times. The reason for suggesting 7 is that the lumen must be reduced by this amount before streamline is altered to turbulent flow by size alone. It appears to be a law of the coronary arteries, however, that the part of the wall in contact with streamline flow remains normal, and if this is so the figure may well be much more than 7. (2) Complete occlusion of a main trunk does not usually stop all flow beyond, because the first branch below the occlusion can reverse its flow and act as a feeder to its parent trunk. (3) Very small branches from the large trunks commonly have a normal structure, whether they arise from the streamline The basis for this from our flow or the turbulent zones. experiments is that the central movement is in the form of a vortex, but this is separated from the arterial wall by a streamline zone (fig. lo). These tiny branches are often the threads by which our life hangs. Late deaths from coronary disease after hypotensive

anaesthesia undoubtedly occur-one is referred to by Gruvstad et al.2 My experience now makes me believe that this is not just a chance association. My letter of May 25 was not intended as an offence to anybody-merely as a warning that the hypotensive state has dangers which are very easy to overlook because the he delaved hv Derbyshire Royal Infirmary, Derby.

cnnRfmncfs mav

some vears.

G. R. OSBORN.

INFLUENZA VIRUS

SIR,ŇThe finding of Stern and Tippett 3 that the 1963 strain of the A2 influenza virus could be grown more readily at 33°C than at 37°C bears out our own experience. In the early part of this year there ample serological evidence in our own, and from other, laboratories of the activity of the influenza " A " virus. Great difficulty was, however, experienced in growing the virus, from swabs taken from the throats of cases, by the normal technique in embryonated eggs at 36°C. At this temperature, a large number of amniotic passages were required before a sufficient titre of virus could be obtained to perform haxmagglutination-inhibition studies. It was then decided to incubate the inoculated eggs at 33°C, and almost immediately several isolations were made was

quite easily. The difficulty encountered with this year’s strain of influenza " A " virus at 36 or 37°C seems much greater than in previous years-indeed, it will be recalled that primary isolation of the original Asian strain in 1957 was achieved with the greatest of ease and regularity at 37°C. This would lead one to suppose that the influenza " A " virus is capable of shifts in biological 2. Acta psychiat. scand. 1962, 3. Stern, H., Tippett, K. C.

37, suppl. 163, p. 83. Lancet, 1963, i, 1301.

character

least as marked as the in antisenic structure. Virus Laboratory, Royal Army Medical College, Millbank,

which

at

more

well-known shifts

occur

London, S.W.1.

P. D. MEERS G. W. THOMPSON.

STERILITY OF EYE MEDICAMENTS

SiR,ŇThe letter by Dr. Phillpotts (June 29) clouds the issue. What are his grounds for suggesting that it is very rare in England for eye lotions, drops, or ointments to be anything but sterile when they leave the dispensary? It was shown in Australia two years ago that dispensing chemists, after the preparation of eye-drops, extremely rarely maintained them at 98° to 100°C for thirty minutes as laid down by the British Pharmaceutical Codex. Consequently these drops were often contaminated and a not uncommon cause of iatrogenic disease. The B.P.C. does not require sterility for eye lotions and not surprisingly admits that mould growth is apt to develop on storage. It is doubtful whether the majority of chemists do better than the legal requirement in this regard. Pseudomonas pyocyanea is a likely contaminant of unsterile eye lotions which, in the presence of

even

minor ocular trauma,

are an

obvious

danger. It would be of interest to know the methods used by Dr. Phillpotts’ dispensers to sterilise eye ointments. The B.P.C. does not require sterility. At our hospital we have tested 81 tubes of 21 different varieties of commonly used drugs produced by 14 different international firms and find that 33% of these eye ointments facturer. It is

are

contaminated when

they

leave the

manu-

unlikely that production methods vary between our two countries, so it is obvious that sterility of eye ointments in England cannot be taken for granted. It is agreed that an antiseptic with antiviral properties would be a boon to ophthalmologists, but a suitable fungicide is also desirable. Adelaide,

D. O. CROMPTON.

South Australia.

PSYCHIATRY AND HOSPITAL ADMINISTRATION

correspondents, I find (June 15) a great disappointment. Being quite newly a principal medical officer when he presented his Maudsley bequest lecture, I flew to London to learn more of my job. I learned that (1) medical superintendents are unnecessary, and (2) the job is better done by the chairman of the medical advisory committee (it happened that I had at another hospital been chairman for five years of a medical advisory committee that had voted unanimously in favour of medical superintendents !). His points about areas of authority, delegation, lines of SIR,-Unlike

some

of your

Dr. Hutchinson’s paper

authority, lines of communication, and joint consultation had already been made from Seebohm Rowntree at the beginning of the century to Dr. Tom Ling of the Roffey Park Institute in the middle. What then is he saying ? I think he is advocating the impermanence of the position, for it is easier to dispose ofa principal medical officer on the grounds of moral turpitude than on those of clinical and administrative incompetence. This implies either the frailty of all men, or the ineffectiveness of our selection system in the mental health service. Dr. Hutchinson argues from the particular to the general in saying that a system that works well at Cane Hill is generally applicable. It would be sheer brutality to load the duties of principal medical officer on to the chairman of our medical advisory committee; for he, on four sessions a week, is responsible medical officer for 500 patients. What more would Dr. Hutchinson have him do ? Dr. Hutchinson is unkind to many principal medical officers. In most hospitals of which I have personal knowledge, this officer is the best clinician and takes his full share of admissions. If I may express a personal view it is this: that a principal

151 medical officer’s job is to get the hospital running so well that it runs without him: that a psychiatrist’s job is to give his patient the individual psychopharmacology and social rehabilitation that he needs to get him out of hospital, even if this means rather less in terms of in-hospital summer holidays and chamber music. Parkside Hospital, R. H. BOARDMAN. Macclesfield.

INVOLVEMENT OF THE JAWS IN BURKITT’S TUMOUR

SIR,-Dr. Lehner (July 6) illustrates the fallacy of building a hypothesis on one " carefully studied case ". It has been the policy of this department to conduct a

examination

of Burkitt’s tumour coming postmortem Mulago Hospital. The high incidence of jaw involvement naturally excited our interest, and an investigation was undertaken to determine the exact site of origin of the tumour in the jaws. It was at once apparent that this information could not be obtained from the advanced jaw lesions, since in these the ramus of the mandible or the alveolar margin of the maxilla is usually partially or completely destroyed, and the surrounding soft tissues, including tongue, salivary glands, muscle, and lymph-nodes, extensively invaded.

meticulous to

of all

cases

at

Three mandibles from cases with loosening of the molar teeth as the only evidence of tumour involvement and one maxilla from a case with infiltration of the soft palate but no loosening of the teeth have been studied. These jaws were fixed in 10% formol saline for about one week, then frozen in an alcohol/dry-ice mixture and serially sectioned on a band saw. The numbered sections were further fixed in a mercurial fixative before being decalcified. The decalcified blocks were embedded in nitrocellulose and sectioned on a sledge microtome. All three mandibles showed complete replacement of the marrow by lymphoma. However, the unerupted teeth, gingiva:, minor salivary glands, and perimandibular soft tissues were tumour-free. The one maxilla sectioned showed two small tumour foci, one in the floor of the maxillary antrum and one in the marrow space of the zygomatic process. In none of these cases was there tumour in the parotid gland. These findings support the radiological evidence of Davies and Davies1 that these tumours begin in the marrow cavity of the jaw. In more advanced cases radiating spicules of bone surround the jaw, indicating that the tumour has burst out through the periosteum carrying subperiosteal osteoblasts with it. Several mandibles and one maxilla from cases of Burkitt’s tumour coming to postmortem without clinical evidence of jaw involvement have been sectioned. In none of these has tumour been found macroscopically or microscopically. Cases of Burkitt’s tumour occasionally present with enlargement of one of the major salivary glands, which may attain enormous dimensions.2 The majority of cases with jaw involvement, however, show no enlargement of the salivary glands. If the tumour arises in the parotid and grows along branches of the maxillary artery to reach the jaws, as Dr. Lehner postulates, why is it not also distributed along the course of the superficial

temporal vessels ? Dr. Lehner states that O’Conor3 found postmortem involveparotid gland in 31 % of cases with jaw tumour and in only 7% without jaw involvement. In fact O’Conor found salivary-gland involvement in 31 % of 13 jaw cases (i.e., 4 cases) and 7% of 15 non-jaw cases (i.e., 1 case). Apart from the statistical insignificance of these figures, they refer to salivarygland involvement (the parotid was involved in only 3 of the total 106 clinical and postmortem cases) and they do not distinguish those cases in which the tumour arose within salivary glands from those cases in which the salivary glands were invaded by an expanding jaw tumour. 1. Davies, A. G. M., Davies, J. N. P. Acta Uno. int. Cancr. 1960, 16, ment of the

1320.

2. 3.

Burkitt, D. Postgrad. med. J. 1962, 38, 71. O’Conor, G. T. Cancer, 1961, 14, 270.

While it is possible that the jaw is occasionally invaded from a salivary-gland tumour, the evidence available at present indicates that these tumours begin within the marrow cavity of the jaw. It is tempting to postulate that the jaw localisation may be related to the unerupted or erupting teeth since the majority of jaw tumours occur at a time when the deciduous teeth are being shed and the permanent teeth are erupting. The higher incidence of jaw tumours in children than in adults with this tumour syndrome may support this hypothesis. However, a number of cases presenting with proptosis have tumour in the upper maxilla without involvement of the alveolus; and the one maxilla referred to above showed small foci in the marrow cavity of the zygomatic and in the floor of the maxillary antrum, but none process in relationship to the teeth. Further postmortem studies of early jaw tumours may help to elucidate this problem. Finally, Sir, may I suggest that you abandon the term " Central African lymphoma " (used in your leading article of July 6). This tumour has a much wider distribution than the term " Central Africa " implies. It occurs in East, West, and South Africa and probably also in New Guinea. At a recent symposium on lymphoreticular tumours,4 it was agreed that this tumour should be called Burkitt’s tumour. This eponym gives due credit to the surgeon who first described this tumour syndrome in its entirety5 and demonstrated its remarkable geographic distribution in Africa .6 78

tumour

Department of Pathology, Makerere University College Medical School, Kampala, Uganda.

D. H. WRIGHT.

CLEFT LIP AND PALATE AFTER THALIDOMIDE

SIR,—The number of cases of thalidomide embryopathy known to us in Japan is increasing. Among the 100 patients onihand at present, there is one of cleft lip and palate associated with a definite history of thalidomide intake during the critical period of pregnancy. The mother, aged 25, was a healthy primipara. There was no family history of congenital malformation. Her last menstrual period was on March 26, 1962. From May 14 until May 22-i.e., from the 49th to 57th day after the last menstrual period-the mother took 2-1g. of ’Isomin’, equivalent to 210 mg. of thalidomide. During the period of the intake she ’

under medical care. On Jan. 8, 1963, she delivered a living female infant weighing 3100 g. The delivery was not complicated. The baby had a cleft lip on the right side accompanied by a cleft palate. Otherwise, there were no malformations typical of thalidomide history, except for a Darwin’s ear was

deformity bilaterally. The critical period of thalidomide intake capable of inducing foetal deformity is from the 35th to 60th day B-11 after the 1st day of the last menstrual period. In this case the mother received thalidomide during the latter half of the critical period. Lenz and Knapp9 described one case of cleft lip with cleft palate, one of spina bifida, and one of osteogenesis imperfecta in which the mothers had taken thalidomide during pregnancy. In each of these 3 cases the exact date of the intake is unknown. In their opinion the association of these malformations with thalidomide intake was probably fortuitous. Schönberg 12 found no case of cleft lip or cleft palate in a series of 55 cases of thalidomide embryopathy. Thus, there has been no case reported of cleft lip and palate with a definite history of thalidomide intake during the critical period. 4. U.I.C.C. Symposium on Lympho-reticular Tumours. Paris, 1963. 5. Burkitt, D. Brit. J. Surg. 1958, 46, 218. 6. Burkitt, D. Brit. J. Cancer, 1962, 16, 379. 7. Burkitt, D. Nature, Lond. 1962, 194, 232. 8. Burkitt, D. Brit. med. J. 1962, ii, 1019. 9. Lenz, W., Knapp, K. Dtsch. med. Wschr. 1962, 87, 1232. 11. Weicher, H., Bachman, K. D., Pfeiffer, R. A., Gleiss, J. ibid. p. 1397. 10 Knapp, K., Lenz, W., Nowack, E. Lancet, 1962, ii, 725. 12. Schönberg, H. Ann. Pédiat. 1963, 200, 60.