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rate five years after operation in MOLONEY’S 9 series of253 inguinal hernias repaired by nylon darns was 0.8%.Some further support for the nylon darn comes from theWest Indies, where LEACOCK and ROWLEY,lO with 348inguinal repairs by a nylon darn technique examinedbetween one and ten years after operation, found arecurrence-rate of 1-4% with 0-9% sinuses; and thesmallest recurrence-rate in the series from the banks ofthe lower reaches of the Thames 2 followed the use of a
nylon darn. The tensile strength of nylon sutures re-moved at abdominal re-explorations even ten yearsafter implantation was shown by BOLONEY 11 to bestill effective. Enduring fibres may be successful inthe repair of hernias not only because the essentialfibrous barrier is formed in the mesh and in the tissuesabout it but also because the darn itself continues to be aneffective barrier, whereas the vegetable and animal fibresare reduced by the action of the tissues within six monthsto ropes of sand.12 (This applies also to plastic grafts forarterial replacement.) The search for other plasticscontinues; and monofilamentous ’Terylene’ or poly-ethylenes such as Marlex ’ 13 as a darn or ready-mademesh may eventually prove to be less affected by thetissues and freer of sinus troubles. The metals have beenused in similar fashion. ABEL and HUNT,14 SHOULDICE,15and RYAN 16 some years ago advocated a darn of stainlesssteel wire; and now LEE McGREGOR joins in recommend-ing this and, in addition, suggests that where the
posterior wall is very weak, the steel wire be reinforcedwith tantalum mesh or polyvinal sponge. KOONTZ hasstrongly advocated tantalum gauze for some forms ofdirect hernia. Metals fragment, and this may lead toweaknesses. Long-term studies are needed on all thesesubstances. As with our outward covering, opinion willbe divided on whether to use something ready-made orto
" tailor " for each individual. There is a move awayfrom braided sutures which seem to be associatedwith a greater liability to sinus formation than are themonofilamentous sutures, be they plastic or metal.MARSDEN makes a careful analysis of troublesome
wound pain; and LEE McGREGOR suggests that this canbest be averted by identifying and protecting the nervesduring the dissection, and that if the ilioinguinal nerveappears to be damaged or caught in the scar it should bedivided lateral to its entry to the inguinal region; numb-ness, he says, is trivial and temporary. Testicular atrophyis best averted by care with the vessels in the cordand by avoiding too tight a repair around the cord. Butif the repair is too loose the way is laid for recurrence.When the coverings of the cord are bulky after reductionof a large hernia they will, if left intact, gradually atrophyand leave a gap; this cause of recurrence can be antici-
pated by clearing away the cremaster, fascia, and fatfrom the upper end of the cord, leaving only the essentialvessels and vas about which a snug repair is made. If thisrepair is carried well up into the muscle and well over the10. Leacock, A. G., Rowley, R. K. ibid. Jan. 6, 1962, p. 20.11. Moloney, G. E. Brit. J. Surg. 1961, 58, 528.12. Douglas, D. M. Lancet, 1949, ii, 497.13. Usher, F. C., Cogan, J. E., Lowry, T. I. Arch. Surg. 1960, 81, 847.14. Abel, A. L., Hunt, A. H. Brit. med. J. 1948, ii, 379.15. Shouldice, E. E. Ont. med. Rev. 1953, 20, 670.16. Ryan, E. A. Surg. Gynec. Obstet. 1953, 96, 343.
medial end of the canal there will be, even years later, nochinks in the fibrous armour through which persistentinternal pressures can thrust.
Hernias recurrent for the third and fourth time havebeen permanently repaired by a well-planned, properlyperformed operation. Knowledge and care can make thefirst time the last time.
Placental TransfusionFEW children’s physicians would dare to transfuse or
withdraw a quarter of a newborn baby’s blood-volumeover five minutes, yet there is convincing evidence thatat birth an infant may lose or gain up to 100 ml. of bloodaccording to whether the cord is tied sooner or later.As early as 1801, ERASMUS DARWIN 1 suggested that theloss or gain of the considerable volume of blood on theplacental side of the circulation might prove to be ofphysiological importance for the infant, and by the endof the century K6STLIN 2 was able to cite nearly sixtyreferences to published work on the subject, beginningwith a characteristically prescient contribution fromARISTOTLE. BUDIN 3 in 1875 had shown that often asmuch as 100 ml. of blood could be extracted from the
separated cord and placenta after birth, and in sur-prisingly close agreement ENGEL 4 found that at birth aninfant might gain up to 100 g. in weight from theplacenta if separation was delayed. These findings,although mentioned in the major textbooks 5 and subse-quently confirmed by investigators employing a varietyof techniques,6 7have not been consistently reflected inobstetric practice, since there has been disagreement asto whether delayed division of the cord is better for theinfant. ENGEL 4 had claimed that the mortality amongpremature infants was halved when division was
delayed, and pointed out that more blood was obtainedfrom the placenta when the conceptus was immature,it has since been shown that the blood-volume of
premature infants tends to be low relative to body-weight. Once the cord has stopped pulsating, gravitydetermines whether blood flows from placenta to foetusor vice versa 9 10; and as a corollary it has been sug-gested that at cxsarean section a baby may actually loseblood to the placenta since he is usually lifted abovethe mother when the cord is tied." There is thus con-
vincing evidence that the notably large variationsin the blood-volume of newborn infants 12 13 may resultfrom variations in the distribution of blood between
baby and placenta; and in addition it has been demon-strated that, if division of the cord is delayed, the baby’svenous pressure after birth will be higher,14 the rise in1. Darwin, E. Zoonomia; vol. III, p. 302. 1801.2. Köstlin, R. Z. Geburtsh. 1898, 39, 98.3. Budin, P. Progr. méd., Paris, 1875, 3, 7, 50; ibid. 1876, 4, 2.4. Engel, G. Zbl. Gynäk. 1885, 46, 721.5. See Leak, W. N. Brit. med. J. 1959, i, 584.6. De Marsh, Q., Windle, W., Alt, H. Amer. J. Dis. Child. 1942, 63, 1123.7. Haselhorst, G., Allmelling, A. Z. Geburtsh. Gynäk. 1930, 98, 103.8. Schulman, I., Smith, C. H. Amer. J. Dis. Child. 1954, 88, 567.9. Duckman, S., Merk, H., Lehmann, W., Regan. F. Amer. J. Obstet.
Gynec. 1953, 66, 1214.10. Gunther, M. Lancet, 1957, i, 1277.11. Crissey, R. R., Knapp, W. L. Amer. J. Obstet. Gynec. 1952, 63, 1059.12. Sisson, T. R., Lund, C. J., Whalen, L. E., Telek, A. J. Pediat. 1959,
55, 163.13. Mollison, P. L., Veall, N., Cutbush, N. Arch. Dis. Childh. 1950, 25, 241.14. Taylor, P. M., Egan, T. J., Birchard, E., Bright, N., Wolfson, J. Acta
pœdiat., Stockh. 1961, 50, 149.
1223
haematocrit after birth will be more pronounced,15 16the total iron stores may be larger,17 and the hxmo-globin level will be greater up to 3 months of age.I8Following up ENGEL’Spioneer work, Dr. BOUND and
his colleagues report in this issue a considerable dropin the death-rate from the pulmonary syndrome of thenewborn after the institution of delayed cord-transectionin a maternity hospital, and they imply (without givingdata) that the incidence of clinical respiratory distresswas also reduced. Since, as they themselves point out,their study was based on a comparison of mortality-rates over consecutive periods, which is a notoriouslyunreliable method of assessing the influence of a par-ticular change in technique, they cannot be said to haveestablished a complete case for routine postponementof cord section (indeed a recent study by TAYLORet ap9 may point in the opposite direction). But withthis reservation their results are impressive and deserveserious consideration by obstetrician and pxdiatricianalike. If tying the cord immediately does increase thelikelihood of the baby’s dying from the pulmonarysyndrome, two explanations are conceivable: the first,that it causes the condition; the second, that a babymay be more likely to die of respiratory distress if
hypovolxmic or anxmic. If tying the cord early is thecause of the respiratory distress syndrome, this couldbe the result of either a failure to recruit placental bloodor a sudden rise in peripheral arterial resistance withresultant left-heart failure, as postulated by GITLIN.20The observations of WOODBURY et al.,21 who, likeASHWORTH and NELIGAN,22 demonstrated no rise inarterial blood-pressure on tying the cord, militate againstthis explanation; but, by inserting a needle into oneumbilical artery, WooDBURY et al. may have decisivelyaltered what they were measuring. As regards the alter-native explanation, the lungs may possibly be more diffi-cult to inflate when blood-pressure is low, as it is whenthe cord is tied early and in the respiratory distress syn-drome,23 though here there is a conflict of evidence.24 25The distress syndrome is thought to be commoner inbabies after an antepartum hxmorrhage, when theblood-loss may be of foetal origin; and, among reportedcases of babies who had lost blood at delivery by acci-dental incision of the placenta during cxsarean section,2 of 11 premature infants died of hyaline membranedisease 2121 though others showed no respiratory dis-tress. It is reasonable to suppose, as JAYKKA 28 hassuggested, that pulmonary blood-flow must increasesynchronously with inflation of the lungs if the lungsare to function satisfactorily; and, since the amount of15. Black, J. A. Personal communication.16. Gairdner, D., Marks, J., Roscoe, J., Brettell, R. Arch. Dis. Childh. 1958,
33, 489.17. Zuelzer, W. W. in Modern Trends in Pediatrics (edited by J. P. M.
Tizard and A. Holzel); p. 116. London, 1958.18. Lanzowsky, P. Brit. med. J. 1960, ii, 1777.19. Taylor, P. M., Bright, N., Birchard, E. Unpublished.20. Gitlin, D. Pediatrics, 1957, 19, 657.21. Woodbury, R. A., Robinow, M., Hamilton, W. Amer. J. Physiol. 1938,
122, 472.22. Ashworth, M., Neligan, G. Lancet, 1959, i, 801.23. Neligan, G., Smith, C. A. Pediatrics, 1960, 26, 735.24. Lewin, R. J., Cross, C. E., Ruben, A., Salisbury, P. Amer. J. Physiol.
1960, 198, 873.25. Daly, I. deB., Daly, A. deB. J. Physiol. 1959, 148, 201.26. Butler, N. R., Martin, J. D. Brit. med. J. 1954, ii, 1455.27. Neligan, G. A., Russell, J. K. J. Obstet. Gynœc. Brit. Emp. 1954, 61,
206.28. Jaykka, S. Acta. pœdiat., Stockh. 1954, suppl. 112.
blood in the lung probably doubles over the time ofdelivery,29 and comprises thereafter about a fifth of thewhole blood-volume,3O 31 it may be very important forpulmonary function that the baby receives a transfusionfrom the placenta of the same amount. The observationsof BONHAM-CARTER et al.,32 showing that distressedbabies are less likely to die when their venous pressureis raised, and of COHNSTEIN,33 who observed that therise in blood-pressure following the initial fall with
respiration occurs only if tying the cord is postponed,may well be relevant. Further evidence comes from thework of MAHAFFEY and ROSSDALE, who in 195934 des-cribed a disease in thoroughbred foals following assisteddelivery which clinically and pathologically resemblesthe pulmonary syndrome.35 They believed that thecause might be the demonstrable loss of a large volumeof blood to the placenta as a result of early division of thecord; and, in subsequent work on newborn lambs,ROSSDALE 35 has shown that removal of blood apparentlyhas different clinical effects before and after expansionof the lungs.From all these results it seems that there are some
grounds for tying and cutting the cord as late as possible;and to achieve this during cxsarean section or when themother’s condition is causing anxiety, the techniquedescribed in this issue by Dr. SECHER and Dr. KARLBERGshould prove extremely useful. They have shown thata satisfactory transfer of blood from placenta to infantis brought about by delivering the placenta with thebaby and by raising the placenta in a funnel so thatblood flows down the umbilical vein by gravity whenthe clamp is released. The time now seems ripe for aproperly controlled clinical trial of late and early cordclamping in relation to immediate neonatal morbidityand mortality.
A Century of SchistosomiasisIT is just over a hundred years now since THEODOR
BILHARZ, performing a necropsy in Egypt, discovereda trematode worm in the portal vein which he namedDistoma hamatobium. Today schistosomiasis threatensto replace malaria as a major scourge of mankind. Com-pared with the enormous strides in malaria control,efforts to eliminate schistosomiasis have been disappoint-ing. Almost fifty years have passed since two Japaneseworkers proved that the mollusc was the intermediatehost; and two years later, in 1915, antimony was firstused successfully in treatment. In 1917 copper sulphatewas introduced as an effective molluscicide. By 1920,therefore, the life-cycle of the worm had been workedout, a promising treatment introduced, and a chemicalfound to control the snail. There seemed every hopethat schistosomiasis would be conquered. But, contraryto all expectations, the control of malaria has proved29. Everett, N.B., Simmons, B.S., Anat. Rec. 1954, 119, 424.30. Karlberg, P., Adams, F. H., Geubelle, F., Wallgren, G. Act. gynec.
scand. (in the press).31. Lagerlof, H., Woerko, L., Bucht, H., Holmgren, A. J. clin. Lab. Invest.
1949, 1, 114.32. Bonham-Carter, R. E., Bound, J. P., Smellie, J. M. Lancet, 1956, ii,
1320.33. Cohnstein, Zbl. Gynäk. 1886, p. 6767.34. Mahaffey, L. W., Rossdale, P. D. Lancet, 1959, i, 1223.35. Rossdale, P. D., Silver, I. A. Personal communication.