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Cæsarean SectionCÆSAREAN section may be preferred as a seemingly

easy alternative to vaginal delivery (though fordifferent reasons) by both obstetrician and patient.Yet the maternal mortality for this operation is stillabout ten times greater than that for vaginal delivery,and in Brooklyn, New York, in 1937-50 caesareansection was a constant factor in about 20% of allpuerperal deaths.l The features which have con-

tributed to the progressive decrease in maternal

morbidity and mortality from caesarean section-

including the use of blood-transfusion, antibiotics,and ergometrine-have also reduced the risk ofvaginal delivery. D’Esopo 2 reported that complica-tions of caesarean section in 1000 cases at the Sloane

Hospital, New York, included the following : puerperalinfection, 107 ; wound infection, 29 ; surgical shock,27 ; thrombo-embolic disease, 24 ; burst abdomen,2 ; intestinal obstruction, 2 ; damaged bladder, 1 ;haemorrhage requiring hysterectomy, 1. MARSHALLand Cox 3 reported that of 7762 caesarean sectionsin nineteen British teaching hospitals during 1943-47the maternal mortality was 0-99%. Such figures area corrective to the view that caesarean section is

preferable to any obstetric operation other than thesimplest type of low forceps and that all other methodsof delivery will become obsolete.4 5The classical caesarean section, which has many

disadvantages, has been largely replaced by the lower-segment operation. In the classical approach thefoetus is extracted feet first and commonly takes deepinspiratory gasps before delivery is complete ; liquoramnii is thus aspirated into the respiratory passagesand fatal atelectasis may result. The incision, inthe anterior uterine wall, is subjected to inter-mittent tension with each " after-contraction " ofthe puerperium. This leads to the formation of a gutteron the under-surface of the scar which may be the

starting-point of rupture in a subsequent pregnancy. sThe uterine scar is exposed to the peritoneal cavity ;and gut may become adherent and later strangulate.Nevertheless the occasional surgeon working underemergency conditions finds this the easier operation,and for his patient it may be the safer. WATERS 7

advocated an extraperitoneal approach, to reducethe risk of disseminating intra-uterine infection ’:but the operation is difficult, and has been abandonedin this country. Occasionally the bladder is damaged ;commonly the peritoneum is opened ; and the incidenceof serious infection is not reduced.Many of the difficulties and dangers of the lower-

segment operation can be avoided by careful attentionto technique, 8The bladder is kept empty by an indwelling rubber

catheter. The peritoneum over the lower segment isincised transversely near the upper limit of its looseattachment, and the bladder is pushed down by verygentle finger separation. A midline catgut traction-suture is inserted in the lower segment, which is incisedprogressively with a scalpel while the muscle is pulledaway from the fcetal head. When the amniotic sac is

1. Gordon, C. A. Amer. J. Obstet. Gynec. 1952, 63, 284.2. D’Esopo, D. A. Ibid, 1950, 59, 77.3. Marshall, C. M., Cox, L. W. Transactions of the 12th British

Congress of Obstetrics and Gynæcology, 1949, p. 30.4. Harris, J. M., Rosenblun, G., Ginsburg, B. L., Stollman, B. D.,

Stenmore, M. S. West J. Surg. 1951, 59, 337.5. Cosgrove, S. A. Amer. J. Obstet. Gynec. 1950, 59, 104.6. McIntyre, D. Proc. R. Soc. Med. 1924, 17, 131.7. Waters, E. G. Amer. J. Obstet. Gynec. 1945, 49, 739.8. Russell, J. K. Lancet, 1955, ii, 322.

9. Feency, K., Barry, A. Brit. med. J. 1956, i, 65.10. Gordon, C. A. Amer. J.Obstet. Gynec. 1957, 73, 65.11. Dewhurst, C. J. J. Obstet. Gynœc., Brit. Emp. 1957, 64, 113.12. O’Dwyer, J. P. Lancet, 1955, ii, 324.

opened the incision is completed by separating thetransverse fibres with digital stretching. With a fingerin the infant’s mouth the head is rotated occiput posterior,the chin is hooked out over the upper uterine flap, andthe head is delivered slowly by flexion with the hand.A head impacted in the pelvic brim can be freed bymild Trendelenburg tilt. Intravenous ergometrine 10 mg.is given and spontaneous expulsion of the placentais awaited. Meanwhile lateral traction-sutures are

placed in the lower segment incision. Commonly theplacenta is delivered by cord traction ; but in cases

where the uterus is atonic this results in profuse hæmor-rhage from the placental site. Continuous sutures inthe lower segment may cause severe ischaemia and theformation of a weak scar ; interrupted sutures of finecatgut are preferable. Aspiration of blood and liquorwhich have spilled into the peritoneal cavity will reducethe incidence of postoperative distension of the bowel.Intravenous fluids are not given as a routine; butwhere much blood-loss is expected, as in placenta prsevia,an intravenous drip should be set up before operation.Prophylactic antibiotics are administered where sepsisis expected-particularly after prolonged labour withruptured membranes.

The risk of ruptured uterus after csesarean sectionis increased by each subsequent pregnancy andvaginal delivery ; by high parity ; by multiple preg-nancy, large foetus, and hydramnios; and byimplantation of the placenta beneath the scar.9In many clinics in the U.S.A. a caesarean-section scaris regarded as an absolute indication for terminatingfurther pregnancies in this way; and in 1954 in

Brooklyn 38-7% of caesarean sections were done forthis reason.10 This will not completely eliminate therisk of scar rupture, since 25% of ruptures followingthe lower-segment operation and 50% of rupturesfollowing the classical operation take place beforethe onset of labour.

Rupture of the classical scar is more dangerous toboth mother and child. DEWHURST 11 reports that in762 pregnancies of women who had undergone theclassical operation the scar ruptured in 17 cases (2-2%).In 100 reported cases where the scar ruptured, the mater-nal mortality was 5 % and the foetal mortality 73 %. In40 % of all cases the placenta overlies the scar. Afterrupture the uterus contracts and retracts, the amnioticsac ruptures, and often the placenta and fœtus are

partly expelled into the peritoneal cavity ; haemorrhagefrom the placental site is profuse, and the patientpresents the picture of severe shock. She has severecontinuous abdominal pain and tenderness ; the foetalheart cannot be heard and the foetal parts may beeasily felt. Intermittent labour pains usually cease,and there may be slight vaginal bleeding. The foetusdies from cord compression, placental separation, andmaternal cardiovascular collapse.

Rupture of the lower-segment scar is less dangerousand less usual. DEWHURST 11 reports 8 cases in 1530pregnancies (05 %). Rupture may be gradual andunaccompanied by dramatic symptoms. Even wheresymptoms and signs are more pronounced and theperitoneum is involved, the foetus is usually-but notalways 12-retained in utero, the placenta is rarelyinvolved, and bleeding is usually slight. The foetal lossis consequently less (12-5%) and in this country nomaternal death has been recorded. In the presence ofa lower-segment scar, therefore, the mode of deliverywill depend largely on the indication for the firstcaesarean section. If this was on account of a recurringcause, such as contracted pelvis or diabetes mellitus, anelective lower-segment csesarean section is indicated.Otherwise vaginal delivery, carefully supervised inhospital, with facilities for immediate transfusion andoperation, is to be preferred. The second stage of labourshould not exceed fifteen minutes, and if necessary,

725

delivery is hastened by episiotomy and forceps. It iswise to palpate the lower segment with two fingers toexclude late rupture during foetal expulsion.

Suspected rupture of the scar is best treated byresuscitation and immediate laparotomy-especiallyif labour is established. After delivery of the foetusand placenta, either the uterus is repaired and thefallopian tubes ligated, or, in the more severe case,subtotal hysterectomy is undertaken.Half the foetal deaths in deliveries by caesarean

section are attributable to the risks inherent in theoperation itself. In Brooklyn in 1954 there were2693 caesarean sections : 2714 infants were deliveredwith 44 stillbirths and 90 neonatal deaths-a peri-natal mortality-rate of 49-4 per 1000 live and stillbirths, which represents an incidence about 55%above the general perinatal mortality for New Yorkcity (GORDON 10). We should therefore hesitate beforedeciding on caesarean section solely in the interestsof the infant.

1. Page, I. H., Corcoran, A. C., Udenfriend, S., Sjoerdsma, A.,Weissbach, H. Lancet, 1955, i, 198.

2. Macfarlane, P. S., Dalgliesh, C. E., Dutton, R. W., Lennox, B.,Nyhus, L. M., Smith, A. N. Scot. med. J. 1956. 1, 148.

3. Sjoerdsma, A., Weissbach, H., Udenfriend, S. Amer. J. med.1956, 20, 520.

4. Smith, A. N., Nyhus, L. M., Dalgliesh, C. E., Dutton, R. W.,Lennox, B., Macfarlane, P. S. Scot. med. J. 1957, 2, 24.

5. Gaddum, J. H., Giaman, N. J. Brit. J. Pharmacol. 1956, 11, 88.

Progress in ArgentaffinomatosisARGENTAFFlNOMATOSIS—the syndrome resulting

from the secretion of 5-hydroxytryptamine by argent-affinomas—is now familiar, though rare. In cases ofobscure cyanosis or flushing and in pulmonary stenosis,it is accepted that abdominal carcinoids come into thedifferential diagnosis ; and the estimation of urinary5-hydroxy-indole acetic acid is established as a valu-able diagnostic meastire.1 2 But of the underlyingbiochemistry and physiology of the process muchremains to be learnt.One of the most interesting aspects concerns the

source of the 5-hydroxytryptamine (5-H.T.). Meta-bolic studies on relatively large series of patients inBethesda 3 and Glasgow, 4 supported by the use ofisotope-labelled tryptophan,3 have shown very clearlythat the 5-H.T. is derived from tryptophan. In somecases a very large proportion of the normal dietaryintake of tryptophan is diverted to this process, andthis, combined with the diarrhoea often present, leadsto a considerable risk of a nicotinic-acid/tryptophandeficiency.4 The conversion of tryptophan to 5-H.T.seems simple enough. Oxidation of tryptophan atC 5 produces 5-hydroxytryptophan, and loss of C02from the carboxyl group produces the correspondingamine, 5-H.T. GADDUM and GIAMAN s demonstratedthe presence of a decarboxylase which accomplishedthe second part of this process, and showed that itsdistribution corresponded fairly well with the sites offormation of 5-H.T. The first part remains elusive.The tryptophan oxidase that would produce5-hydroxytryptophan has never yet been demon-strated in animal tissues. Tryptophan incubated withrat-liver slices, for instance, undergoes no 5-hydroxyla-tion. One of the cases in the Glasgow series 4 wastherefore of especial interest, for 5-hydroxytryptophanin substantial quantities appeared in the urine,apparently from renal metastases of the tumour. Thisis valuable confirmation of the reality of the postu-

lated route of formation. DALGLIESH and DUTTON 6

go further, and deduce that the tumour, and so pre-sumably the normal argentaffin cells from which thetumour has arisen, must be capable of this essential5-hydroxylation of tryptophan. SJOERDSMA et al.3failed to demonstrate such an action in tumour tissue,but so fruitful is this hypothesis that their findingsshould be re-examined. It follows, if DALGLIESH andDUTTON are right, that the major function of theargentaffin cells is not the local release of 5-n.T.(though this may be one of their functions) but themanufacture of its precursor, 5-hydroxytryptophan,for circulation to various other cells which decarboxy-late it and turn it into the active hormone. Amongother things, this would account for the fact that,though 5-H.T. is produced apparently by severaldifferent kinds of cells, no other kind of tumour

produces excess of it. The body’s total production of5-H.T. is presumably limited by the availability of theprecursor, and only the argentaffinoma can produceexcess of the precursor. The elimination of 5-H.T. byoxidation to 5-hydroxy-indole acetic acid (5-H.I.A.A.)is effected by an amine-oxidase present especially in thelungs. MACFARLANE, et awl. made the interestingsuggestion that some of the discrepancies between theintensity of symptoms and the level of hormoneproduction (one of their patients excreted 600 mg. of5-H.I.A.A. a day but had no relevant symptoms exceptslight diarrhoea) might be accounted for by an adaptiverise in the amine-oxidase content of the lungs. Butthis possibility has been eliminated by DAVisorT andSANDLER,7 7 who showed that the lung amine-oxidaseremains at normal levels. The relation to 5-H.T.secretion of the most striking feature of the

syndrome-the vasomotor changes which accountfor the flushing and cyanosis-is uncertain.4 Nothing further seems to have been learnt of the

origin of the endocardial lesions. Their constant

appearance downstream from the main tumourmasses makes it difficult to believe that we are not

seeing a direct effect on the endocardium of sometoxic material produced by the tumour. But what ?5-H.T. seems the only possible answer, yet no actionof 5-H.T. that would account for its damaging theendocardium is known. Its presence in high contentin the platelets does not seem to damage them, andthere is no evidence from the few adequate post-mortem studies reported 8—10 that platelet depositionor thrombosis play any part. One can only assumethat 5-H.T. in high concentration has some unrecog-nised action on the endocardium, or that some unrecog-nised secretion of the tumours is the culprit. Eventhat most satisfactory observation of GoBLE et al.11—namely, a substantial removal of 5-H.T. from the bloodduring its passage through the lungs in one patient(thus accounting, it seemed, for the difference betweenthe lesions in the left and right hearts)-has beenchallenged by SJOERDSMA et al.,3 who found nodifference between the 5-H.T. content of pulmonary-artery blood and femoral-artery blood. Amongconfusing observations it is a relief to find in theGlasgow series studies of gastric function (high pepsin6. Dalgliesh, C. E., Dutton, R. W. Biochem. J. 1956, 64, 481.7. Davison, A. N., Sandler, M. Clin. chim. acta, 1956, 1, 450.8. Spain, D. M. Amer. J. Med. 1955, 19, 366.9. Gable, A. J., Hay, D. R., Hudson, R., Sandler, M. Brit. Heart J.

1956, 18, 544.10. Smith, J. P., Campbell, A. C. P. J. Path. Bact. 1956, 72, 673.11. Goble, A. J., Hay, D. R., Sandler, M. Lancet, 1955, ii, 1016.