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to know that there are by now many engineers of good academicstanding who would wholeheartedly devote their research

interests to the problems of biomechanics.I am surprised at the comments made by Mr. Charnley

about the reluctance of the engineers to cooperate with thesurgeons. It was the Institution of Mechanical Engineers whoorganised a symposium on biomechanics in 1959-not the

British Orthopxdic Association. Mr. Charnley was invited tocontribute a paper to that symposium in collaboration withtwo engineers. In my opening remarks on that occasion Istressed the need for cooperation between surgeons and

engineers.In 1956, when I gave three university public lectures on the

mechanics of the human body and the behaviour of metalsused in implants, invitations were sent to all those medicalinstitutions whose members might be expected to be interested.The audience, with the exception of five orthopaedic surgeons,consisted solely of engineers.

I can assure Mr. Charnley that if he wishes to employ on apermanent basis a qualified engineer with biomechanicalinterests I can give him at least three names and addresses.I suggest that this course would be an improvement on Mr.Charnley’s proposal to rely on "the remarkably large numberof fellows and members of the B.O.A. with natural mechanicaltalents". It takes as long to train a qualified engineer as totrain a surgeon-my point is perhaps best illustrated by the"success" of the original Judet prosthesis and the variousnailing techniques of the neck of the femur. Let us drop theamateur’s approach and try, if not to understand the problemsinvolved, at least to develop some appreciation of theirexistence.

It is essential for the surgeon to develop a dual approach tohis problems. One is to apply existing knowledge to everydaycases as they arise, and the second is to embark on long-termbasic research. It is in the latter that the engineer is of value.However, it seems in my experience that the surgeon isinterested only in an immediate answer to his day-to-dayproblems and does not appreciate the necessity for further andoften lengthy research.With reference to Dr. Scales’ letter, standards can be of

value if based on experimental data and consequently if usedwith some understanding of their limitations. One can onlystandardise knowledge which already exists and one cannot

produce standards by the mere fact of gathering several peopleinto a committee.

Your annotation will have been of the greatest value if itarouses sufficient interest to further the course which Ihave been advocating for years-the setting up of a centralresearch institute of biomechanics in this country.

Biomechanical Laboratory,Civil Engineering Department,

King’s College, J M ’7.——-London, W.C.2. J. M. ZAREK.

SIR,-Your annotation of Feb. 11 and Dr. Steele’sletter of Feb. 18 make it clear that there are many peoplewho would welcome an organisation, consisting jointly ofmedical men and engineers, whose purpose would be thepooling of technical knowledge in the wide area in whichbiology and engineering overlap.The initiative has in fact already been taken, and the

Biological Engineering Society, which has this as itsmain object, came into being last year.The Society holds scientific meetings (the first was at the

National Institute for Medical Research, Mill Hill, in Octoberand the second at Guy’s Hospital in January) at which papersare read and equipment demonstrated; and it provides oppor-tunities for discussion of mutual problems between its mem-bers, who include engineers, physicists, biologists, and medicalmen. Affiliated membership is also available to scientificinstitutions and to commercial organisations. The councilof the Society intends to establish a central information service,

which will store and make available information on apparatusand components, fields of special interest, and current literature.A journal is also being considered.

Association with other bodies, as envisaged in your annota-tion, is included in the aims of the Society. Its honorarysecretary is Dr. A. Nightingale, Physics Laboratory, St.Thomas’s Hospital, S.E.I, from whom further informationmay be obtained.

J. M. ZAREK.

Biomechanical Laboratory,Civil Engineering Department,

King’s College,London, W.C.2.

RONALD WOOLMERPresident,

Biological Engineering Society.Royal College of Surgeons,

London.

1. Morris, J. N., Crawford, M. D. Lancet, Jan. 7, 1961, p. 47.2. Morris, J. N. ibid. 1951, i, 1, 69.3. Wilens, S. L. Amer. J. Path. 1947, 23, 793.

THE MAMMARY SOUFFLE

WALTER SPORRG. A. MACGREGOR.

Holy Cross Hospital,Haslemere,

Surrey.

SIR,-We were interested in your annotation of Feb.25, having lately seen a case in which this sign was clini-cally relevant. Although unaware of the prior referenceto it, we also called the murmur an " internal mammarysouffle " in view of its association with lactation.

In 1959 a primipara of 20 with postpartum pyrexia wasadmitted to this hospital because she had mild anaemia, a

palpable spleen and a localised, hissing, parasternal murmurin the second left intercostal space. Blood-cultures weresterile, and the fever settled without antibiotics in 14 days. Themurmur was systolic extending into diastole, and it seemed tolag behind the heart-sounds. Firm pressure with a bell stetho-scope temporarily silenced it. It was therefore exocardial andunlike a ductus-arteriosus murmur. It resembled a uterinesouffle and we attributed it to increased flow in the mammaryartery because the patient was lactating unusually freely.A month later the patient was well, but the murmur wasunchanged. Lactation ceased after 12 weeks, and examinationthen showed that the murmur had disappeared. Her spleenwas also impalpable, and its earlier enlargement was ascribedto iron deficiency. The murmur was not heard in 10 motherssubsequently examined after childbirth.We thank Dr. K. M. McNicol for referring the patient to us.

ATHEROSCLEROSIS AND

CORONARY OCCLUSION

SIR,-The data in the second table (Coronary-arterydisease, 1908-56) of Professor Morris and Dr. Crawford’sletter do not necessarily reinforce the hypothesis thatatherosclerosis has declined in severity over the pastforty to fifty years.

According to Professor Morris’s previous analyses 2 ofnecropsy records at The London Hospital for the years 1908-13and 1944-49, the severity of atherosclerosis had substantiallydeclined in the forty years between these periods. It wasassumed that the criteria for grading atherosclerosis had beenessentially the same during both periods. This assumption isnot a strong link in the argument and it can hardly be validatedby now comparing the 1908-13 records from this hospital withthe results of the 1954-56 National Necropsy Survey. Withsuch a diversity of participants, the standards for gradingatherosclerosis in the survey were probably less consistent withthe 1908-13 standards than those in use at the same hospital inthe 1944-49 period.

Another possible flaw in the argument is that the nutritionalstate of the subjects in the groups under review may have beenquite different. Without the benefit of modern therapeuticagents and recent surgical advances, a patient in the 1908-13era may well have died sooner after the onset of his mortalillness than his counterpart in the 1944-49 or 1954-56 periods.It has been shown that the inanition of chronic diseasesmobilises lipid from the atherosclerotic plaque. Thus the sub-jects in the 1944-49 and 1954-56 groups would have had alonger period of terminal malnutrition, in which to resorbatheroma lipids, than those of the 1908-13 group. Hence,

556

postmortem appearances in hospital patients might give thefalse impression that atherosclerosis in the general populationis less severe nowadays than it was fifty years ago. In thefuture this problem could possibly be resolved by making aquantitative assessment of coronary atherosclerosis at necropsyin subjects who have died suddenly from trauma but who areotherwise healthy. A quantitative index for coronary athero-sclerosis could well be adapted from that formulated by Dr.Holman and his associates 4 for atherosclerosis of the abdominalaorta.

In the face of a spectacular increase in the incidence ofcoronary occlusion during the last half-century, the suggestionthat there has been a corresponding decline in the severity ofcoronary atherosclerosis is so unexpected that it surely requiresmore exact confirmation before it can be accepted. Even if theconclusion is correct, it cannot be inferred that atherosclerosis

causing stenosis and occlusion of the coronary lumen is an

essentially different disease to non-stenosing atheroma of thecoronary wall. A small atherosclerotic lesion can precipitateocclusion just as effectively as generalised disease of the wholecoronary vasculature.1 5 The critical factor, which determinesocclusion, is merely the direction of enlargement of the lesion-i.e., the degree to which the atherosclerotic process expandsinwardly rather than up or down the arterial wall. Thus the

underlying cause of coronary occlusion is still coronaryatherosclerosis.

C. W. M. ADAMS.

Laboratory of Pathology and Histochemistry,National Institute of Arthritis

and Metabolic Diseases,National Institutes of Health,

Bethesda, Maryland.

4. Holman, R. L., Brown, B. W., Gore, I., McMillan, G. C., Paterson, J. C.,Pollak, O. J., Roberts, J. C., Wissler, R. W. Circulation, 1960, 22, 1137.

5. Crawford, T., Dexter, D., Teare, R. D. Lancet, Jan. 28, 1961, p. 181.

AN AID TO THE DIAGNOSIS OFHYPOFIBRINOGENÆMIA

L. S. DEANE.Withington Hospital,Manchester.

SIR,-I was interested to read Dr. Aidin’s letter

(Feb. 25); he is to be congratulated on his attempt to helpclinicians to remember what kind of bottles are requiredfor the estimation of blood-fibrinogen and the performanceof the clot-observation test. I feel, however, that he may beunderestimating the ability and memory of the cliniciansthough I have no doubt that his aide-memoire wouldsometimes be useful.

Most cases of hypoiibrinogenaemia in obstetrics followaccidental haemorrhage of the severe mixed or concealed

variety; and, from a practical point of view, fibrinolysinsrarely cause hypofibrinogenaemia. Few investigators have beenable to demonstrate the presence of these substances. The

diagnosis of hyponbrinogenaemia may be made when theconditions producing a fall of fibrinogen are remembered andthe blood-fibrinogen is serially estimated or the clotting-timeobserved; these conditions are accidental hxmorrhage,retained dead fretus or missed abortion, and amniotic embolism,in order of descending frequency.

I would strongly disagree that fibrinogen should be givenwhen the blood-fibrinogen falls to 200 mg. per 100 ml., sincethis would mean that all cases of hyponbrinogensemia wouldreceive this treatment. There is adequate evidence that,provided intravenous oxytocics are given at the end of thesecond stage, there is rarely any further uterine haemorrhage,even though there may be haemorrhage from the needle

puncture points in the skin. In general, fibrinogen should begiven when operation is necessary, where there is extensive

genital-tract injury, if anxsthetic agents which relax uterinetone are used, or if third-stage hxmorrhage continues in spiteof the use of oxytocics, and when the fibrinogen level is below100 mg. per 100 ml. If fibrinogen is required (and 1 Americanauthor found it necessary to give fibrinogen in only 7-4% of casesof accidental haemorrhage), then it is better to use triple- orquadruple-strength plasma,_since fibrinogen is difficult to getinto solution and, since it is prepared from large pools of plasma,is said to carry a greater risk of homologous serum jaundice.

The clot-observation test is useful where facilities are notavailable for fibrinogen estimation. If a filmy clot develops, butdisintegrates within twenty to thirty minutes, then the fibrinogenconcentration of the blood is below 100 mg. per 100 ml. If noclot forms at all, then the concentration of fibrinogen is below60 mg. per 100 ml. and, since hypofibrinogenxmia develops infrom two to thirty-six hours (usually within six hours) of theonset of placental separation in accidental hamon-hage,frequent clot-observation tests or fibrinogen estimations of theblood are required.

It should not be forgotten that a fall in the blood-prothrombinactivity accompanies that in the fibrinogen. The prothrombinactivity should also be estimated and, if necessary, intravenousphytomenadione (vitamin Kl) can be given.

1. Lancet, 1960, ii, 1352.2. Brit. med. J. Jan. 21, 1961, suppl. p. 15.

DYSPNŒA DUE TO SUBCLINICAL AMŒBIASIS

R. ELSDON-DEW.

SIR,-I wonder whether Dr. Hamilton and Dr,Lutwyche 1 would be kind enough to explain themechanism by which Entamaeba histolytica caused the

dyspnoea complained of by the patient. If this is an

allergic phenomenon, have they any evidence, other thanthe test of cure by drugs whose whole range of activity isstill unknown, that the allergen was, in fact, E. histolytica)

Amcebiasis Research Unit, R ELSDON-DDurban.. EW.

FIND THE LADY

SiR,—I refer to the distribution of the E9 million

retrospective payments to hospital medical staff. It is

quite clear that the distribution scheme, recommendedby the working-party as

"

extremely fair and reasonablehas achieved the remarkable feat of favouring practitionersat opposite ends of the ladder. Consultants with meritawards and the lower grades are to receive surprisinglylarge sums, while consultants without awards come outrelatively badly.Why is this ? At the special representative meeting last

September, the Representative Body, relieved to knowthat the mysterious proposed scheme carried a guarantee(" extremely fair and reasonable "), quite properlyapproved the scheme, along with all the other recom-

mendations, in good faith and without question. Someof us, unable to find the catch, had been shrewd enoughto take the working-party’s report to our accountants orgroup finance officers, only to find that even " our’

experts could only scratch their heads and wonder.Like schoolboys unable to solve difficult problems, those of us

sufficiently interested can work backwards from the answers inan attempt to solve the mystery. The inescapable fact is thatthe formula inherent in the scheme has worked overtime for

practitioners with low (pre Royal Commission) salaries whowere given relatively large percentage increases by the RoyalCommission. Fair enough, possibly, but why the fine dividendsfor our most highly paid consultants ? The trick here is to

split the awards away from the basic salary and each ills-

tinguished consultant is thus divided into two bits, a major anda minor. A questionable manoeuvre and quite contrary to theRoyal Commission’s observation that " awards are thus simpba part of remuneration

"

(para. 214 of the report). The e&Kof this is dramatic. To take a simple example, the consultantwith C award, and at the top of the scale, we find that in respec,of his award he is to receive E408 as compensation for a salaryincrease (1956-60) of E250, but in respect of his basic increaseof E800 he receives only E405. (I have adjusted the figure 10

the very top of the scale.)It can be said, of course, that the awards did not receit.

any interim adjustments in 1957 and 1959. In total tho‘c

payments for the C award would amount to E88 (5% off500