intrauterine transfusionthepresent pregnancywill offer little information of value until after...

POSTGRAD. MED. J. (1966), 42, 755.

INTRAUTERINE TRANSFUSIONJ. KARNICKI, F.R.C.O.G.

Consultant Gynaecologist and ObstetricianC. A. HOLMAN, M.R.C.P., F.C.Path.

Consultant Pathologist

Lewisham Hospital, London, S.E.13

THE treatment of haemolytic disease of the newbornhas advanced dramatically in recent years.The analysis of the liquor amnii, (Bevis, 1956;

Liley, 1961, 1963; Walker, 1962), has permittedmore precise assessment of the state of the foetusin utero. For very severely affected babies an earlyinduction of labour at 32 to 34 weeks of pregnancywas practised but with poor results. The survivalrate of such premature infants, badly affected byhaemolytic disease, was extremely small.

In order to prolong intrauterine life of theaffected foetus, Liley (1963) introduced intra-peritoneal foetal transfusion. Blood introducedinto the peritoneal cavity becomes absorbed intothe foetal circulation and helps the foetus to surviveuntil reasonable maturity is reached.

Intrauterine TransfusionIn 1964 we reported our first attempts at intra-

peritoneal transfusion of the foetus (Holman andKarnicki, 1964). Since then we have treated 54infants and have met a number of complications.The purpose of this communication is to report onour further experience and the changes in our viewsand techniques.We commence by assessing the past history of the

patient and her pregnancies, which should be ascomplete as possible. It is not sufficient to knowthat there was a stillbirth delivered at 36 weeks;what one needs to know is as precisely as possibleat what maturity the infant was seriously affectedand when it actually died. Sometimes it is possibleto know when intra-uterine death had occurred, orthat the foetus had become less active, some weeksearlier. Since complications in pregnancy oftenlead to iso-immunization the influence of these inrelation to the fate of previous pregnancies mustalso be considered. What we are seeking to forecastis whether an intra-uterine transfusion is likely tobe needed, at what stage hydrops foetalis is likely toappear, when delivery will be possible and whetherany other problem, such as placental insufficiencyor a tendency to premature delivery, may bepresent.The antibodies are titrated in saline and in

albumin and by the indirect Coomb's technique and

most regard is paid to the latter. Antibody titresare a very rough guide and whenever possible we seekto correlate the titre in the previous pregnancy withits effects on the infant.The present pregnancy will offer little information

of value until after quickening. Loss of the foetusbefore 20 weeks is very rare but from that time thepatient should be watched with extra care and theantibody titre checked regularly.We believe that spectrophotometric examination

of the liquor amnii is a necessary preliminary tointra-uterine transfusion but we cannot agree thatamniocentesis should be practised routinely onante-natal patients with iso-immunization. Sinceour first report (Holman and Karnicki, 1964), inwhich we referred to the danger of foetal exsan-guination, about 500 amniocenteses have beenperformed here and two foetuses have been lost bypuncture of a vessel on the foetal aspect of theplacenta. We have no doubt that amniocentesisshould be restricted to those patients in whom thehistory or the antibody titre indicates a risk of still-birth. In practice this means all patients with ananti-D titre of 1 in 32 or more by the indirect Coomb'stest plus those with a lower titre who have had aprevious stillbirth or severely affected liveborn infant.In many cases the need for amniocentesis is clear atthe beginning of the pregnancy and the real problemis not whether, but when, to do it. When we havethe history of a previous stillbirth as a guide weusually commence amniocentesis at least a monthbefore the maturity at which intra-uterine deathoccurred and not later than 26 weeks. If the previousaffected infant was liveborn we defer amniocentesisuntil 28 - 30 weeks unless the antibody titre isexceptionally high. In the case of a first affectedpregnancy the antibody titre is the only guideavailable and one can only judge on the degree ofaffection seen in other foetuses at the same titre.Our anxiety in regard to amniocentesis rests

largely on the risks of puncturing the placenta.After about 30 weeks of pregnancy it is oftenpossible to exclude anterior placenta by palpationand to find a safe puncture site. Between 20 and30 weeks clinical assessment of the placental siteis difficult or impossible. We have been dissatisfied

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756 POSTGRADUATE MEDICAL JOURNAL December 1966

0.90 : _:'__

:. :

0.70

o. ,-i . ...-.:-I::.... .I..i. j.......:....: :.:.. ......:QSC.. :' :e':_, _....

0.6 -trl

0.40 ---- l-r -------

0.3,1

0,20I

__01__ _0 _ j,Zi.:i.i:I l1;:._.) . -_-----_-_--- l

0.- *-t

--

0.0 4- .t- ----!----

. ,_..:. ._. .._ _.__. ..I.{.:-Absorption Curvt of Liquor Amnil

b0expecte-d tntr t amnitc vi y ortqurenter,btnt pas withrouttBliruin

Peak op,atdwensity difnterencrbetweenA (actualanapprec4lngati450inJ aand B (the redficnl ate450n

blood l 0145 if tinsexampto no

700 600 500 400 300 mp

Fig. 1

with the results of radio-isotope localisation andcannot always afford to wait several days for ananswer. We therefore attempt amniocentesis witha pl hypodermic needle which, in general, wouldbe expected either to enter the amniotic cavity or toenter, but not pass through the placenta. Believing,as we do, that women with anterior placentas havean appreciably greater risk of a foetomaternalblood leak from ante-natal palpations, we do notthink that the chance of entering it with a needleadds greatly to that risk. If the amniocenteses havebeen performed without drawing blood it will bepossible to proceed to intra-uterine transfusionwhenever indicated but if blood has been drawnthe placenta must be localised and we now submitour patients to arterial placentography and findthat this is most helpful.

0.90 .0.8 .. Haemogiion -1_n

0.7 '--''-K-----0.67__.0, --0l---

0.6-·-------ok- ---O.O

0.15 --

> .' ' ' / . I'.. . . . lo

0.0

o. -___---'-- ..... .... ............

0 08-- t i..0.06 ---- 52M-

0.0

-

' :' - '- ', ' ' ' ' -j

0.04 -

0.02 . Absorption Curve ofLiquor-AmniI. .contolining bilirubin and haemoglobin

- ------Expected curve ir same: liquor --

i without hoemoglobin

ioi700 600 500 400 300 mu

Fig. 2-Note that the haemoglobin peak at 410 mp over-laps the bilirubin peak at 450mp interfering withthe method of reading described in Fig. 1. Thesegment of the curve between 520 and 490 mp isunaltered by the presence of haemoglobin.

Although the method described by Liley (1961)for estimating the absorption peak at 450 mp (seeFig. 1) is usually reliable we have found that thepresence of haemoglobin and associated pigmentsin amniotic fluid may make an accurate assessmentimpossible at a time when it is essential. Knox,Fairweather and Walker (1964) showed that thepart of the curve between 490 and 520 mp is relatedto the height of the 450 mp peak above the baselineand that it is unaffected by the presence of haemo-globin (see Fig. 2). Dr. D. N. Whitmore hasanalysed our curves and has shown that the differencebetween the optical density readings at 490 and 520mp multiplied by a factor of 1.49 normally yieldsthe same figure as does Liley's method. Because



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December 1966 KARNICKI AND HOLMAN: Intrauterine Transfusion 757

NAME209---------------^___9______-_9__---3-3R.T.-^.^E.D.D. 7_i-g.: :

-^_:_-:-'- CHART derived from that produced by Lil Icy but extended backward s fro mw_ 27 to 20 weeks. Peak optical density plotted against maturity of foetus.

I ---^ - - --1^^[ O -7~~ L IDUPPER ZONE: likelhood ofl - - - -;

ydrops toetalls orO _.3i_-- ^,_____ *^ .- - --: sn tillbirth.

-07_--_-_----- i

-7-L7.

o DO inTa-i_:MIDDLE ZONE: likelihood of liv 7 -.

03 I--- I-I- - -ifonts- with hoemolytic disease. Th

Note t -t {tere~ safairmohigher the level the more severe the

nfants [ynotbeaveOWER ZONE: pnntd-tse.Note that there is a fair amount of

Infants may not behave as predicted.EEKS 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38

Fig. 3

there are occasional discrepancies we calculate bothfigures and accept the answer if they agree.

In the interpretation of the results we have beenguided by Liley's analysis and plot the calculatedpeak at 450 mi against the maternity in weeks onsemilogarithmic graph paper. Fig. 3 shows Liley'schart extrapolated backwards from 27 to 20 weeks.Although our results correlate fairly well withLiley's we have found that there is a significantoverlap in the lower middle zone between unaffectedand moderately severely affected infants, and thathydropic infants can yield peaks below the upperzone.Once amniocentesis has been performed it should

usually be repeated at weekly intervals. In thecourse of two weeks an infant can pass from thenormal to the severely affected group.The decision to perform an intra-uterine trans-

fusion is fairly easy to make if it rests on a suddenincrease in the 450 mu peak into the area of thechart associated with hydropic and stillbornfoetuses. Since hydrops foetalis is generally irrever-sible and is the chief cause of death in this groupof foetuses, intra-uterine transfusion is only likelyto be successful if given before the foetus becomestoo anaemic. To determine the latest time at which

transfusion will succeed is quite difficult andrequires consideration of the course of the presentand previous pregnancies and of the antibodytitres. We think that, where there has been aprevious stillbirth, it is better to start before theperiod at which the previous infant's movementsbecame weak. Where there has been no previousstillbirth the problem usually affects foetuses ofabout 30- 34 weeks' maturity in which the risksof intra-uterine transfusion are not great and weare tending to the view that, in a doubtful case,there may be less risk to the foetus in transfusingthan in waiting.The major deterrent to intra-uterine transfusion

is the position of the placenta. In pregnanciesbetween 20 and 30 weeks it may be impossible toreach the foetal abdomen without penetrating theplacenta and we regard this as an unacceptablerisk. In pregnancies over 30 weeks the anteriorplacenta does not occupy the whole of the anterioraspect of the uterus and it is usually possible byarterial placentography to discover an area throughwhich the transfusion can be done with safety.

In our first report we were considering foetusesof about 32 - 34 weeks and were able to place aTuohy needle in the foetal abdomen without using



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POSTGRADUATE MEDICAL JOURNAL

Urografin as a marker for the foetal gut. When lessmature foetuses were presented for this treatment itbecame clear that swallowed Urografin was ofgreat value as a marker when foetal bones werebarely visible: it also permitted more accuratepuncture of the lower abdomen, thus avoidingdamage to liver and spleen. In those early days wedid not have the use of an image intensifier andtelevision set linked to the X-ray unit. Once thisbecame available we found that we could use it asLiley now did and usually manage without ordinaryX-ray pictures providing that the foetus hadswallowed the Urografin. The foetal gut is clearlyvisible on the television screen and the puncture ismuch easier.

TechniqueOur present technique starts with the injection of

15 - 20 ml. of Urografin into the amniotic cavity onthe day before the transfusion. The foetus swallowsthis and concentrates it at first in its small intestineand later in the large bowel. Even a foetus assmall as 21 weeks will do this successfully. If theUrografin is not apparent in the gut it is probablethat the foetus is hydropic, the alternatives beingthat it is anencephalic or has duodenal atresia. Onone occasion, however, we found that the Uro-grafin could not be seen in the foetal gut until aboutthree days after injection; the foetus had haemolyticdisease but was not hydropic and was otherwisenormal.

It is usually easier to aspirate liquor than toinject fluid into the amniotic cavity. As the foetushas a tendency to block the needle with its limbs,which a sharp needle could easily penetrate, theUrografin might be injected into foetal tissueinstead of the amniotic cavity. We therefore usean arteriography trocar and cannula for the injectionof the Urografin. The trocar is removed as soonas the amniotic cavity is entered and the contrastmedium can then be injected safely.For the actual transfusion it is best for the foetus

to be in a lateral position. On the day of thetransfusion the patient is asked to lie quietly on herback in the hope that the foetus will settle into thelateral position in the hollow beside the maternalspine. In this position the needle can pierce themother's abdomen directly above the foetal abdomenand pass easily into the foetal peritoneal cavity.When the foetus is in the posterior position theneedle has to pass between the limbs which makesthe operation rather difficult. Furthermore, theplacenta is likely to be in the anterior position andlimit access. Obviously it is equally difficult totransfuse if the foetus is completely anterior. Therelation of the foetal position to the area of theanterior surface free from placenta is of great

importance in the successful performance of thetransfusion. For example, one patient had ananterior placenta which covered everything exceptthe left side of the fundus; the foetus was in the leftsacro-lateral position and the foetal head wasdirectly under the only possible site for puncture.We postponed the operation until the next day bywhich time the foetus had turned to the left occipito-lateral position and its abdomen was easily accessible.Whenever the foetal abdomen is difficult of accessit is better to postpone the operation than topersevere.

Premedication consists of pethidine 100 mg. andpromazine 50 mg. intramuscularly one hour beforetransfusion. Antibiotic cover is provided by fourmega-units of penicillin and one gram of streptomy-cin divided into four doses over 24 hours.The operation takes place in the X-ray department

with strict aseptic precautions. A local anaestheticis given through a 1- needle at the site chosen forpuncture. This is determined by the position of thefoetus and placenta, aiming at the lower quadrantof the foetal abdomen in order to avoid the liverand spleen which are usually enlarged. The foetalbladder occupies a large part of the lower adbomenbut there appears to be no risk attached to punctur-ing this organ.The skin is nicked with a knife before the Tuohy

needle is introduced. A 6" Tuohy needle has provedsatisfactory providing that the sharp edges on allaspects of the orifice have been blunted. The Tuohyneedle is introduced into the uterine cavity andunder television screening the needle is directedtowards the foetal abdomen. Small babies are verymobile and may have to be transfixed through thebuttock with a separate needle to reduce movement.It is possible to feel the various structures throughwhich the Tuohy needle passes; the foetal abdomenoffers little resistance and one is aware when theneedle enters the abdominal cavity. In some casesascitic fluid can be aspirated and is easily recognisedas it is more deeply pigmented and more viscousthan the liquor. When the needle is in the rightposition the catheter will pass through it easily.We use a 24' "Pink Portex" nylon catheter, O.D.1.02 mm. If the needle is in a tissue the cathetercannot be pushed in at all and if it is in the bladderit does not pass very easily. Once the whole catheterhas been introduced, 2 ml. of Urografin are injectedthrough it and a characteristic picture of contrastmedium between the coils of gut, under thediaphragm and outlining the foetal abdomen, isseen on the television screen. The blood is nowinjected and is followed by 2- 3 ml. of Myodil, aninert oily radio-opaque solution which will remainin the peritoneal cavity indefinitely and will helpto guide the Tuohy needle during the next intra-

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KARNICKI AND HOLMAN: Intrauterine Transfusion 7

TABLE 1

INTRA-UTERINE TRANSFUSIONS FROM NOVEMBER 1963 TO MARCH 1966

Total number of Transfusions 84

Total number of Patients 54

Foetal survival Foetal Loss

27 (50%) 27 (50%)

Stillbirths 14Neonatal Deaths 9Abortions 4

uterine transfusion without preliminary injection ofUrografin. The Tuohy needle is then gently with-drawn leaving the bulk of the catheter inside thefoetal abdomen.The amount of blood introduced varies with the

size of the foetus. We try to guess the weight ofthe baby and give the appropriate amount of packedRh-negative red cells of the same ABO group as themother.At 21 weeks the size is about 400 g. and we give

about 40 ml. of blood. At 32 weeks the size may be1,600 g. and 160 ml. would be given. Usually thesequantities are as much as the abdomen can hold.The intrauterine transfusion is repeated every twoweeks. The rate of growth of the baby from 24 to28 weeks is approximately 400 g., from 28 to 32weeks approximately 500 g. and from 32 to 36weeks approximately 700 g. The placenta does notgrow so rapidly and is proportionately bigger theearlier the pregnancy. The volume of blood in theplacenta at 28 weeks will probably be double thatin the foetus whereas at 36 weeks may well be nearlyequal. The haemoglobin level achieved will there-fore be lower in the less mature foetus than in themore mature foetus.Between 20 and 30 weeks of pregnancy we now use

a self-retaining catheter made by Dr. J. D. Irving(1966) to allow a larger quantity of blood to beintroduced during the course of a few days. Thiscatheter is based on the same idea as is the pig's tailurethral catheter and has been left in for 2 or 3 daysin several patients without evidence of any ill-effects. We are aware of the danger of infection andhave maintained the antibiotic cover.

ResultsTable 1 shows the results of intra-uterine trans-

fusion from November 1963 to March 1966. Weperformed 84 intra-uterine transfusions on 54 babiesand saved 27 of them.

Table 2 shows the rate of survival as we went onwith the operation. Until September 1965 we had asurvival rate of nearly 60%. From about that timewe accepted more severe cases and attempted muchearlier transfusions. The earliest we did was 21weeks. One of the patients had five transfusions, thefirst one at 25 weeks, but we failed to save thishydropic baby which was born at 36 weeks. Thisattempt to save babies early in pregnancy haslowered the survival rate to 50%.

Table 3 shows the result of intrauterine trans-fusion in relation to previous obstetric history.Two-thirds of our cases had bad obstetric histories.They had previously lost babies or had had verybadly affected infants requiring exchange trans-fusion. One-third of the patients were in the firstaffected pregnancy. The results of each group areapproximately the same; namely about 50%perinatal mortality; the proportion of hydropicbabies is even higher among the first affected babies.These results are in line with Liley's (Liley, 1961)observation that one-third of stillbirths due torhesus immunisation occur amongst the firstaffected pregnancies.

Table 4 shows the results of intrauterine trans-fusions in relation to the duration of pregnancy.When intrauterine transfusion was given after 30weeks of pregnancy we saved two-thirds of thebabies. Below 30 weeks we only saved three out of19.The next two Figures 4 and 5 show the peak

optical density in relation to duration of pregnancyof successful and unsuccessful cases respectively.In the successful group most of the patients are inthe upper zone and the duration of pregnancy is over30 weeks, a few cases are at 27, 29 and 30 weeks ofpregnancy and a few in the upper middle zone. Inthe unsuccessful group most are in the upper zoneand are under 31 weeks of pregnancy.Looking at the proportion of foetal haemoglobin

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TABLE 2

RESULTS OF INTRA-UTERINE TRANSFUSIONS FROM NOVEMBER 1963

No. of No. of Babies Foetal LossI. U.T. Patients Alive

Total SB ND Ab

September 1965 46 34 20 (59.9%) 14 (40.1 %) 7 7

March 1966 84 54 27 (50.0%) 27 (50%) 14 9

TABLE 3

RESULTS OF I.U.T. IN RELATION TO OBSTETRIC HISTORY

No. of Cases Alive Foetal loss HydropsBad Obstetric History 35 18 17 (12)First Affected Baby 19 9 10 (8)

TABLE 4

RESULTS OF INTRA-UTERINE TRANSFUSION IN RELATION TO DURATION OF PREGNANCY

A

A A

A A A A

A A A A

Survival- A A A A

A A A A

3 A A A A A A A A 24

16 M M SB SB SB SB SB SB SB SB SB ND 11

M SB ND SB ND SB ND NDLoss-

M SB ND ND ND SB

ND

Weeks of pregnancy- 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35

A = Alive birthM = MiscarriageSB = StillbirthND = Neonatal Death



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NAME0.9 R.T.E.D.D9 -_0S 11. 1 IBABIES SURIVING0.7 - _-._.____.:_ __:_ ._

O ' e f . ___ __ ____........

.2----::::-_____ ;'..-._____.___._______

~. ..... . , , . :Fi. :::.0

0.0

.06.0 -.........

.0 - ----4- -1--- ---e--- ----_-_Indicates the last peak optical

transfusion 1 1 I I

02WEEKS 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38

Fig. 4

to total cord haemoglobin, Figure 6, we can say thatthe transfusion was justified in almost every case.Case No. 4 shows 40% of foetal haemoglobin. Thefirst recording of the optical density peak was 0.33but at the time of transfusion the optical densitywas 0.081: This error was due to plasma in theliquor. The haemoglobin level of 40% shows thatit was as well we did the transfusion because thechance of survival when the haemoglobin is under50% is poor.Case 9 is a mystery. The husband is heterozygous.

The second child was rhesus-negative but deeplyjaundiced at birth. She had lost her third childwhich was rhesus-positive. The optical densitylevel was rising steadily and entered the uppermiddle zone; the antibody titre was also rising.The foetus had an intrauterine transfusion at 34weeks and a deeply jaundiced rhesus-negative babywas born and required three exchange transfusions.There was no ABO incompatability nor any otherrecognisable abnormality.

Table 5 shows the analysis of foetal loss. Threechildren died from prematurity. Intrauterine trans-fusion had been difficult and had required prolongedmanipulation. This may have caused prematurelabour.

We lost one child as a result of cardiac arrestduring exchange transfusion. Cardiac massage wastoo vigorous. Severe bruising of the heart occurredand the child died from cardiac failure.The other child was lost because of haemorrhage

from the umbilical artery, which had been catheter-ised in the development of a new technique forexchange transfusion.

All the stillbirths and 3 of the neonatal deathswere due to hydrops foetalis. This is the largestsingle factor responsible for failures. Once hydropicchanges have taken place intrauterine transfusionhas little chance of saving the baby.

ComplicationsMaternal complications have been surprisingly

few and have been largely due to anterior placenta.One patient had an intraperitoneal haemorrhage asa result of the puncture of the uterine wall directlyover the placental site with a Tuohy needle. Theuterine musculature at the site of placental attach-ment is more vascular and can contract less wellthan that elsewhere.Two patients became shocked when the Tuohy

needle pierced the placenta but responded to bloodtransfusion. We believe that it is necessary to



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NAME 7f77E.D.D. 0___I ------- -----l---- ....

0. -- --- __ --FOETAL LQSSgEE ;:!-:': i;;:!., -_0. -- _I_ ____ ___

__

T0*p on

i niaei - eac -a s sh -- ---- - - - -___

....---.-'~'~'-: ;::::.'.................

.03------- ---- ---- ---- ---- ___ _ ____--__--.^--. ____ __

0 T-e point indicated in each case istltelost peak optical density before thefirst intro uterine transfusion.0 indicates hydrops foetalls

^

WEEKS 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38

Fig. 5

know the location of the placenta before operationand to avoid puncturing it.We have sought for evidence of other compli-

cations such as infection and amniotic fluidembolism but have found no evidence of them.

Table 6 shows the number of patients who hadpremature onset of labour. Two of these startedlabour before the infant was transfused and twoothers had had previous spontaneous prematuredeliveries. Three infants were hydropic and this, inour experience, predisposes to premature labour.Prolonged manipulation during the operation wasprobably responsible for the premature onset oflabour in two cases. In four cases we could find nocause other than the intrauterine transfusion,which could be held responsible for the prematureonset of labour.

In one case a new antibody (anti Jka) appearedin the mother after an intrauterine transfusion withJka positive blood and made the selection of afurther donor difficult. (Kelly and Kenwright, 1966).

Foetal complications were more numerous. Onfour occasions the autopsy showed previous punc-ture or laceration of the liver which had healed. Inthree stillborn macerated foetuses there wereadhesions between the small intestines and clotted,

I5O FOETAL Hbl TOTAL Hb::]

140

130

120

110

100

90

80

60

40

30

10

CASE No. I 2 3 4 S 6 7 8 91011 12131415161718192021222324252627

Fig. 6-Cord blood haemoglobin levels



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TABLE 5

CAUSES OF FOETAL Loss WrrH I.U.T.

No. of Cases SB ND Ab

Prematurity 3 3

Hydrops 20 15 3 2

Death due to cardiac arrest during exchangetransfusion 1 1

Death due to ruptured umbilical artery duringexchange transfusion 1 1

Abortion, macerated 2 2

Total number 27 15 8 4

TABLE 6DAYS OF ONSET OF LABOUR AFTER I.U.T.

NUMBER OF TRANSFUSIONS 84

Days after I.U.T. 1 2 3 4 5 6 7 8 9

Perinatal Loss 2 1 1 1 1 1 2

Alive 1 2 1

unabsorbed blood. This latter may make punctureson the television screen difficult to interpret.On many occasions the needle and catheter

entered the foetal bladder but no infant suffered asa result of this. In one case the pleural cavity waspunctured and outlined with urografin withoutevidence of subsequent ill-effects. We also managed,in a particularly difficult case with anterior placenta,to put a Tuohy needle into the foetal skull, presum-ably through a suture, and injected urografin. Thisinfant showed no neurological abnormalities atbirth and is now four months old and appears to bedeveloping normally.About 10 inches of nylon catheter snapped off

and was left inside one foetal abdomen. The childis now 18 months old and shows no sign of anyabnormality. It is to avoid this that we adviseblunting the inner aspect of the tip of the Tuohyneedle. Animal experiments were performed by thecourtesy of the Institute of Child Health and havesuggested that the nylon catheter will be quiteharmless.

Further ManagementWe have endeavoured to deliver these infants by

the vaginal route after surgical induction and havenot performed Caesarean sections unless indicatedfor obstetric reasons. Delivery has usually beeneffected at about 36 weeks except in one case wherethe infant was small and induction was delayed anextra week.

After birth these infants still require exchangetransfusions to clear the bilirubin and a few of themhave been poorly for some time but have eventuallydone well. One has required operation for bilateralinguinal hernia and also had a persistent jaundicefor about two months.When these infants are born they are usually

anaemic but not seriously so. The bilirubin level ishigh and sometimes higher than one sees in severehaemolytic disease. The direct Coomb's test may benegative or show a mixture of positive and negativecells. The clinical condition of the infants is oftenless satisfactory than would be expected by thehaemoglobin level. Despite this and the degree of



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jaundice we have usually succeeded in rescuingthese infants with two one-pint exchange trans-fusions. These infants may have very high levels offree antibody and several of them have destroyedall their newly formed red cells so that at aboutsix weeks of age we have been obliged to give atop-up transfusion. This has been given by theintraperitoneal route and the absorption has beenquite satisfactory.Most of the surviving infants have been watched

and so far none have shown any evidence of deafnessor spasticity and are all making normal progress.One required operation for bilateral herniae andalso had persistent jaundice for about two monthsbut now has no detectable sequelae.

SummaryBetween November, 1963 and March, 1966, 54

foetuses were given intrauterine transfusions and27 of them survived. The technique used is des-cribed and the indications and complications arediscussed.

Our thanks are due to the many obstetricians whohave referred their patients to us. The work entailedhas put extra burdens on many of our colleagues and thestaff of the maternity, paediatric, pathology andradiology departments, to all of whom we are greatly

indebted; above all we must acknowledge the great helpgiven by Miss A. Austin and our radiologists Dr.N. A. W. Morrison and Dr. J. D. Irving.

REFERENCES

BEVIS, D. C. A. (1956): Blood Pigments in HaemolyticDisease of Newborn, J. Obstet. Gynec. Brit. Emp., 63,68.

HOLMAN, C. A., and KARNICKI, J. (1964): Intra-uterineTransfusion for Haemolytic Disease of the Newborn,Brit. med. J., i, 594.

IRVING, J. D. (1966): A Self-retaining Catheter for Intra-uterine Foetal Transfusion, Brit. med. J., i, 1228.

KELLY, J., and MARGARET KENWRIGHT (1966): Personalcommunication.

KNOX, E. G., FAIRWEATHER, D. V. I., and WALKER, W.(1965): Spectrophotometric Measurements on LiquorAmnii in Relation to the Severity of HaemolyticDisease of the Newborn, Clin. Sci., 27, 147.

LILEY, A. W. (1961): Liquor Amnii Analysis in theManagement of the Pregnancy Complicated byRhesus Sensitisation, Amer. J. Obstet. Gynec., 82,1359.

LILEY, A. W. (1963a): Errors in the Assessment ofHemolytic Disease from Amniotic Fluid, Amer. J.Obstet. Gynec., 86, 485.

LILEY, A. W. (1963b): Intra-uterine Transfusion ofFoetus in Haemolytic Disease, Brit. med. J., ii, 1107.

WALKER, A. H. C., and JENNISON, R. F. (1962): Ante-natal Prediction of Haemolytic Disease of Newborn,Comparison of Liquor Amnii and Serological Studies,Brit. med. J., ii, 1152.



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