j. perinat. med. preterm premature rupture of the

10
Theunissen et al, Neonatal outcome in PROM 423 J. Perinat. Med. 17 (1989) 423 Preterm premature rupture of the membranes: neonatal outcome in 215 cases of an active conservative management Ingrid Theunissen and Michel van Lierde Unit of Obstetrics, St. Luc University Hospital, Brussels, Belgium 1 Introduction Premature rupture of the fetal membranes (PROM) leads to two main perinatal problems: prematurity and infection [3]. Prematurity occurs because usually labor begins shortly after the rupture [8]. Infection is the consequence of an open amniotic fluid cavity allowing germs to contaminate both the mother and the fetus [20]. In the literature, there is a lack of consensus about the attitude to adopt towards premature rupture of membranes [7J. The obstetrician is confronted with the choice of an optimal follow- up either with or without tocolysis [19, 22], an- tibiotic prevention [20] and hyaline membrane disease prevention by glucocorticoids [3, 4], de- pending on the risk for the neonate and the mother. In the "Cliniques Universitaires S t Luc Brussels" an active conservative management is the option taken. After ten years of practice, we have eval- uated our results by analyzing the perinatal out- come and also by comparing the premature neo- nates after PROM with a control group. 2 Methodology Two hundred and fifteen women between 24 and 36 weeks of pregnancy with premature rupture of the membranes (PROM) were admitted in this study. Diagnosis of PROM was based on patient's story, sterile speculum examination showing pooling amniotic fluid, and microscopic examination for "ferning". At admission, a cervical culture for group β streptococcus was performed. An ultra- Curriculum vitae INGRID THEUNISSEN was born in Genk, Belgium, in 1963. She obtained her medical degree from the University of Louvain Medical School, with highest honors in 1987. She is currently doing her clinical residency in ob- stetrics and gynaecology. In addition, she is doing research in perinatal me- decine. sound examination and an electronic heart rate fetal monitoring was utilized to assess fetal well being. Criteria of exclusion were: major fetal congenital anomalies, fetal death, fetal distress, multiple pregnancies, women in labor and any obstetrical reason for immediate delivery such as vaginal bleeding or evidence of chorioamnionitis. Treatment consisted in bed rest at the hospital, antibiotics continuously given (ampicillin 3 χ l g IVD or erythromicin 4 χ 500 mg in case of al- lergy), and intravenous tocolysis by ritodrine if labor began. No vaginal desinfection was per- formed. Glucocorticoids ( -methasone 12 mg/day IM for two days repeated once a week) were given only before 32 weeks and by the discretion of the attendant physician. Follow-up of the patients consisted of measuring the maternal temperature, evaluating uterine 1989 by Walter de Gruyter & Co. Berlin · New York

Upload: others

Post on 21-Apr-2022

5 views

Category:

Documents


0 download

TRANSCRIPT

Page 1: J. Perinat. Med. Preterm premature rupture of the

Theunissen et al, Neonatal outcome in PROM 423

J. Perinat. Med.17 (1989) 423

Preterm premature rupture of the membranes: neonatal outcome in215 cases of an active conservative management

Ingrid Theunissen and Michel van Lierde

Unit of Obstetrics, St. Luc University Hospital, Brussels, Belgium

1 Introduction

Premature rupture of the fetal membranes(PROM) leads to two main perinatal problems:prematurity and infection [3]. Prematurity occursbecause usually labor begins shortly after therupture [8]. Infection is the consequence of anopen amniotic fluid cavity allowing germs tocontaminate both the mother and the fetus [20].In the literature, there is a lack of consensusabout the attitude to adopt towards prematurerupture of membranes [7J. The obstetrician isconfronted with the choice of an optimal follow-up either with or without tocolysis [19, 22], an-tibiotic prevention [20] and hyaline membranedisease prevention by glucocorticoids [3, 4], de-pending on the risk for the neonate and themother.In the "Cliniques Universitaires St Luc Brussels"an active conservative management is the optiontaken. After ten years of practice, we have eval-uated our results by analyzing the perinatal out-come and also by comparing the premature neo-nates after PROM with a control group.

2 MethodologyTwo hundred and fifteen women between 24 and36 weeks of pregnancy with premature ruptureof the membranes (PROM) were admitted in thisstudy.

Diagnosis of PROM was based on patient's story,sterile speculum examination showing poolingamniotic fluid, and microscopic examination for"ferning". At admission, a cervical culture forgroup β streptococcus was performed. An ultra-

Curriculum vitae

INGRID THEUNISSEN wasborn in Genk, Belgium, in1963. She obtained hermedical degree from theUniversity of LouvainMedical School, withhighest honors in 1987.She is currently doing herclinical residency in ob-stetrics and gynaecology.In addition, she is doingresearch in perinatal me-decine.

sound examination and an electronic heart ratefetal monitoring was utilized to assess fetal wellbeing.Criteria of exclusion were: major fetal congenitalanomalies, fetal death, fetal distress, multiplepregnancies, women in labor and any obstetricalreason for immediate delivery such as vaginalbleeding or evidence of chorioamnionitis.Treatment consisted in bed rest at the hospital,antibiotics continuously given (ampicillin 3 χ l gIVD or erythromicin 4 χ 500 mg in case of al-lergy), and intravenous tocolysis by ritodrine iflabor began. No vaginal desinfection was per-formed.Glucocorticoids ( -methasone 12 mg/day IM fortwo days repeated once a week) were given onlybefore 32 weeks and by the discretion of theattendant physician.Follow-up of the patients consisted of measuringthe maternal temperature, evaluating uterine

1989 by Walter de Gruyter & Co. Berlin · New York

Page 2: J. Perinat. Med. Preterm premature rupture of the

424 Theunissen et al, Neonatal outcome in PROM

tenderness, and performing fetal heart rate mon-itoring twice a day. Maternal leucocytosis andblood sedimentation speed was measured everytwo days. Once a week an ultrasound examina-tion was performed to check fetal well being. Acervical/vaginal culture was also done once aweek to certify a local sterilization. In case ofresistance to ampicillin, the antibiotic treatmentwas adapted.

Pregnancy was terminated in case of suspectedchorioamnionitis (based on any of the followingsigns: maternal fever greater than 38 °C; leuco-cytosis superior to 15000; uterine tenderness; foulsmelling amniotic fluid discharge), fetal distress,labor despite tocolysis, and when gestational agereached 37 weeks. Antibiotics were given duringseven days after birth to all patients. The latencyperiod is the time between membrane ruptureand birth. A latency period of less than two daysis considered a failure of conservative manage-ment.

Results were evaluated by the neonatal outcome:prematurity, birth weight, Apgar score at 1 and5 min, incidence of neonatal hyaline membranedisease (HMD), neonatal infection, and earlyneonatal death (first week of life). Diagnosis ofhyaline membrane disease was based on clinicalevaluation and on characteristic lung radiogra-phy; wet lung, transcient respiratory distress, andpost-anoxic distress were diagnosed seperatefrom HMD.Neonatal infection consisted of a positive centralculture such as blood, cephalo-rachidian fluid orurine, or a clinical evaluation showing evidenceof infection (leucocytosis, response to anti-biotics, ...).Neonatal outcome was compared to neonataloutcome of babies born prematurely for anotheretiological reason; each premature neonate fol-lowing PROM was matched with a prematureneonate of the same birth age and year of birthin order to compare similar neonatal manage-ment. The benefit of pregnancy prolongationafter PROM and the group of neonates born at37 weeks of gestation (not premature) were notconsidered when compared to the control group.

Statistical analysis consisted of Chi-square testsof independence performed on groups separatedby the procedure CROSSTAB of the statisticalpackage SPSS [26].

3 ResultsFrom 1978 to 1987, 215 women with single preg-nancies and PROM entered this retrospectivestudy. Gestational age ranged from 26 weeks to36 weeks of amenorrhea, 113 PROM cases oc-cured before 35 weeks.Reasons for termination of pregnancy and theoverall neonatal results are listed (table I). Inour series we had no congenital malformationand no prenatal death.Pregnancy age at membrane rupture is a majorfactor in determining the outcome (table II). Thelatency period decreases with advanced gesta-tional age. Suspicion of chorioamnionitis is sig-nificantly more frequent at low gestational age.The overall neonatal outcome is highly signifi-cantly (P < 0.01) related to gestational age. Inthe group of PROM occuring at 35 and 36 weeksof gestation, there is no neonatal death, noHMD, and only one case (1 %) of neonatal in-fection.Glucocorticoid treatment in PROM occuring be-fore 33 weeks of pregnancy was administratedin 28 cases out of 58 (48.3%). No difference inneonatal outcome are found respectively withand without treatment: rates of hyaline mem-brane disease (17.9% vs 20.0%), of neonatalinfection (21.4% vs 26.7%) and of neonataldeath (10.7% vs 3.3%) are similar. The rate ofsuspected chorioamnionitis is also similar in thetwo groups (35.7% vs 36.7%).When pregnancy is terminated because of thesuspicion of chorioamnionitis, the neonatal out-come is compromised; the incidence of neonatalinfection is significantly (P < 0.001) related tothe suspicion of chorioamnionitis (table III). Sev-enty cases (32.6%) of PROM had a prolongedlatency period (> 7 days). When comparing thepregnancy outcome with PROM having ashorter latency period, we found no difference.Especially, the incidence of chorioamnionitis(14.5% vs 24.3%, respectively in the short andprolonged latency groups) and of neonatal in-fection (6.9% vs 12.9%) are not statistically dif-ferent.When pregnancy termination was motivated bya gestational age of 37 weeks, (N = 46, 21.4%)fetal grwoth seems to be slowed down. Indeed,the incidence of birth weight inferior to the tenthpercentile was significantly (P < 0.001) more fre-quent in the group reaching 37 weeks of gestation

J. Perinat. Med. 17 (1989)

Page 3: J. Perinat. Med. Preterm premature rupture of the

Theunissen et al, Neonatal outcome in PROM 425

Table I. Premature rupture of the membranes:

Termination of pregnancy:— suspicion of chorioamnionitis— 37 weeks reached— failure of tocolysis— pathologic fetal heart rate— othersNeonatal results:— prematurity:* before 37 weeks* before 35 weeks* before 33 weeks— birth weight:* < 1000 g* < 1500 g* <2000g* <2500g— Apgar scores < 7:* at 1 min* at 5 min— Hyaline membrane disease— Neonatal infection— Neonatal death

Conservative management,

PROMbefore 35113 cases

317

62103

1068551

8265885

713115184

weeks

27.4%6.2%

54.9%8.8%2.7%

93.8%75.2%45.1%

7.1%23.0%51.3%75.2%

62.8%27.4%13.3%15.9%

2.5%

overall results

PROMbefore 37215 cases

3846

113135

1698551

82660

111

993415194

weeks

17.7%21.4%52.6%

6.0%2.3%

78.6%39.5%23.7%

3.7%12.1%27.9%51.6%

46.0%15.8%

7.0%8.8%1.9%

(N = 9,19.6%; versus N = 4, 2.4% in the groupnot reaching 37 weeks).When PROM led to premature birth, the pre-mature neonates before 33 weeks of gestationdid not differ from the control premature neo-nates (table IV). When birth happened before 35weeks and before 37 weeks, there is a lowerincidence of HMD and neonatal death in pre-mature neonates following PROM compared tothe control group.

4 DiscussionThe first problem relating to PROM seems to beinfection, maternal and/or neonatal. The studiesof JOHNSON [18], MILLER [20] and BLACKMON [3]show that the later the PROM occurs during thepregnancy, the smaller is the overall risk of in-fection. This is in agreement with our results.However, according to others, pregnancy agemodifies the risk of chorioamnionitis but not theneonatal sepsis [1].

The controversy about the benefit versus the riskof delaying labor after PROM is the main prob-lem concerning the management of PROM. Ac-cording to the literature, the risk of chorioam-nionitis is variously related to the latency period:many authors find no relationship [6, 14, 18, 20,28, 36, 38] while others find a negative relation-ship [1, 9, 12, 16,33,34].Similar controversial results are found about theincidence of neonatal infection, but the actualconclusion seems to be that there is no relation-ship between the length of the latency period andthe neonatal infection [1, 3, 9, 16, 28, 30]. Wefind that a prolonged latency period (> 7 days)does not increase the risk of chorioamnionitisnor the risk of neonatal infection.The benefit of conservative management lies inthe reduction of HMD, a major complication ofprematurity. A recent report [3] shows the posi-tive effect of a prolonged latency even if previousstudies tend to find no relationship [1, 9, 11, 19,23, 34]. Our results however, also show a trend

J. Perinat. Med. 17 (1989)

Page 4: J. Perinat. Med. Preterm premature rupture of the

426 Theunissen et al, Neonatal outcome in PROM

CO

I"cdα•α&α0

ΟΡ*PH'S"cd

ο8§7αι— ι

S

*0α>"οοQ

^ί·ΚΟ

co

•3<υ

m

Ι(D

m

mm

COI(Nen

100tN

1ωooCS

£<S

?f

1I I

ON

CN

I I/ζ

0^

2

IIζ

eS

sI I

Z

8 88 8 8888 88 8 8 8v v v « 5 « 5 . v . . v v v v v v v v v

PH PH PH C C 1 PH 1 1 PH PH PH PH PH PH PH PH PH

«ooor- O C N O O S O o o ooo«o > o c ? s o o ot-oom S O O O O C N C N ^ H I I O O C N O C — C N O ^ O(N«r )T-H m»o v o ' l ( N es

oo C5 ^f Γ"- O"N ^H m CN m ι ι co co es ^o oo m co *»Ή <οesvo^-H mu-i v o ' l es es

m e s ^ e s o m v o v o C T N T - H I oeses^o e S O e s ^ t oe s ^ t m τ-ir-ivo o o » o l THIO Tf

τ-ιο^ο v o v ^ o m m e s ^ i O - ^ - H ^ O O o m ^ - i e s oτ-neS'^H m ^ i e s ' e s e s

rss g°i-o g & P ossss ^S * ,., «s

co f** m es m co Ό co t**· m cn m r*^ co m es co es co Ό* j* Ό es Ό T-H c3> oo oo m vo f*~ oo c~^ *o es es ^H

<rHr-H TH eseses ^τ-nes T H ^ H

co

1 s |^ 'S s |α 1 s ^

* Jll u l | j i• ΓΗ r? Λ co ^"^ *En ^ "" *^< o *""* ""p, c?^ c ? . | - 2 ' 2 ^ c o ^ " i o O O l ^ ^ ^ ^ . .G § ^ ^

0 ) V ( S | A p M C n t £ 3 C M O Q Q n * * * ^ S w w w w < J n _ » + j S ^π ^

S l l l t f l l l l l ^ l 1 * * * * 1 * * 1 1 l

J. Perinat. Med. 17 (1989)

Page 5: J. Perinat. Med. Preterm premature rupture of the

Theunissen et al, Neonatal outcome in PROM 427

Table HI. Effect of chorioamnionitis on neonatal outcome

ChorioamnionitisN = 38 7.7%

No chorioamnionitisN = 177 82.3%

CHi2

Prematurity:* before 37 weeks* before 35 weeks* before 33 weeks

Birth weight:* < 1000 g* < 1500 g* < 2000 g* <2500g

Apgar scores < 7:* at 1 min* at 5 min

Hyaline membrane diseaseNeonatal infection

Neontal death

382717

49

2127

2613

3

9

0

100.0%71.1%44.7%

10.5%23.7%55.3%71.1%

68.4%34.2%

7.9%

23.7%

0.0%

1315834

4173984

7321

12

10

4

74.0%32.8%19.2%

2.3%9.6%

22.0%47.5%

41.2%11.9%

6.8%

5.6%

2.2%

P < 0.001P < 0.001P < 0.001

P < 0.05P < 0.05P < 0.001P < 0.01

P<0.01P < 0.001

n. s.

P < 0.001

n. s.

of decreasing incidence of HMD with prolongedlatency, but it is not statistically significant(P = 0.079 for PROM before 35 weeks).

In order to accelerate lung maturation, theadministration of ß-methasone is recommended[29]. The majority of reported studies find nodifference in the incidence of HMD when corti-costeroids were given [3, 4, 13, 19, 38]. Ourresults are in agreement with these studies. But,according to SPINNATO [32] these results are notto be considered because the treatment is appliedto a low risk population and needs, for furtherevaluation, to be applied where the potentialbenefit of lung maturation really exists. Corti-coids are known to be related to an increasedrisk of infection, and in a situation such asPROM where infection is threatening it may bedangerous to use them. For some authors glu-cocorticoid administration increases the mater-nal infection risk but not the neonatal infectionrisk [1], while for other authors it increases theneonatal but not the maternal infection risk [31].Other authors find that glucocorticoid adminis-tration does not increase any infection risk [38],and finally, there are authors who find an in-creased maternal and neonatal infection risk [3,24]. We do not find any increased incidence ofchorioamnionitis nor neonatal infection when

patients received ß-methasone. Since we observeno benefit in glucocorticoids administration andthere is doubt about the infection risk, we rec-ommend to not use them.When chorioamnionitis is clinically suspected,pregnancy should be stopped. The increased riskof neonatal infection associated with chorioam-nionitis seems generaly accepted [2, 3, 20] butthe relation with neonatal death is still contro-versial [16, 34, 40]. Our results show that clinicalsuspicion of chorioamnionitis is related with ahigher incidence of neonatal infection but notwith higher neonatal death rate.Hypoplastic lungs after prolonged PROM is welldescribed [26, 37]. For some authors, PROMdoes not affect the growth process [3,18] but forothers, PROM slows the growth [5, 35]. In ourstudy we have no prenatal death, no congenitalmalformation, but fetuses seem to be slower intheir growth. Our control group compares thepremature neonate after PROM with a controlpremature neonate. The results show less HMDand a lower rate of neonatal death after PROM.The principle that PROM decreases the risk ofHMD [3, 9] and the results of BLACKMON [3]who finds a decreased perinatal mortality are inagreement with our results. MOBERG [21] findsan increased incidence of neonatal infection fol-

J. Perinat. Med. 17 (1989)

Page 6: J. Perinat. Med. Preterm premature rupture of the

428 Theunissen et al, Neonatal outcome in PROM

3cd

d8

1Dci,

|8

•JH

21ωcd

"cdd8d83

8

^0ωg

1o3"cd§§'sd

tcd

gOU

1

^d

•su

Q

«Ν^

S

coP!||

zJ21

co<D1Ja

»2o

%OPH·PH

1

χ*t*^ζ:

2I I

Z

co

ONVO

7

fN

u

to

IIZ«ro(D

CO

£H

S

§

6O

xO

to00

000

I Iz

S

11

10

10ooII

ffiυ

8"

I Izίgcoco21

g1o

soPHPH

1cd

0s

p

^Tt

IIz-p•0

τ— 110

IIZ

»O tO IO T-H *OO 0 0 0 0

. 0 0 0 t o .C PH PH PH dd PH d OH

^ g g g §2 es es 2Γ"·- NO NO es CD ^? T-H NO t"**es -xt r- NO es es

τ - Η τ - n e S T - H CO τ— 1 T-H ON T-HT - H « x f C - - T - H U N C O C O T-H

g ^ g g g g g g ^

• x f « o « o o N c o o \ oo es'T-H CO tO IO T-H T-H

O O V O O O O C O <O O Oe s v o o O N C O TH T-H Tf

IO »O IO0 0 0

ς ο ι Λ & τ ΐ γ « 5 « 3 γ «5 γd d d P H d d P H d PH

ο ^ ο Ν ο ^ ο ^ ο ^ ο ^ o^ 0s- 0s-

e s » o e s v o o o t ^ T-H ON co

τ - Η \ ο ο ο ι > t o e s co r* T-HT-H co tn r- tn es es

χ Ο χ Ο χ β χ Ο Ν°Νθ χΟ χΟ ΧΟ0s· 6s 6s 0s« N N 6s ON ON

Ο Ν Ο Ι — · o \ t o t — ο ·co vo oo NO co T-H es

o o v o t ^ e s ΟΝΟ Ό c^ ·es to c^ to co T-H T-H

t » « 5 < / 5 c « 0 2 C « 00 09 C«

d d d d d d d d dχ Ο χ Ο χ Ο χ Ο χ Ο χ Ο χΟ χΟ χΟ

Tf1 co οο C3 Ό t*** ON ON ^fes" t> T-H ο to NO es T-Hes ^O ON Ο Γ~~· co ^r T-H es

^

T - H C O t O O N O - O O 00 to ΟT - H C O - x t ^ · C O T - Η T-H T-H

χ Ο χ Ο χ Ο χ Ο χ Ο χ Ο χΟ χΟ χΟ

r ^ r ^ T - Η θ - x t T — ι «ο to oo« ο θ Ν - x f o d es'r^ to to t-^

o o t o o o o e s - x f co co τΐ-es ^t to Tt eS τΗ τ-Η

(D00cd α

^ .8 -B^ jj ^

S o o o o 8 'l -1 4 ^ Ί^ S ) g o o o o d | ^ 2

rt Cd ^ Ctf ,— κ d d^ 2 j « . j t J t e O j t J t ^ O O^ Η * # # # P H * * >\ δ SPQ <ί κ ^ Jz;

J. Perinat. Med. 17 (1989)

Page 7: J. Perinat. Med. Preterm premature rupture of the

Theunissen et al, Neonatal outcome in PROM 429

Table V. Overall neonatal outcome compared with the literature data

HMD

Neonatalinfection

Neonataldeath

Our resultsIncidence

7%13%

9%16%

2%3%

Literature dataDate of PROM

before 37 weeksbefore 35 weeks

before 37 weeksbefore 35 weeks

before 37 weeksbefore 35 weeks

Incidence

14%12.8%80%8.5%

30.1%14%21%

3.3%4.5%15%3.1%

16%

Date of PROM

26-36 weeks26-36 weeksbefore 32 weeks

before 37 weeks28-35 weeks26-34 weeks26—36 weeks26-32 weeks

Ref.

[10][38][19]

[38][39][29][10]

[1][21][16][16][29]

lowing PROM, which contradicts the findings ofCURET [9]. When we compare premature neo-nates after PROM to the control premature neo-nates, there is no difference in the infection risk.Our management of PROM which consists ofan active and conservative management differsfrom the actual approach recommended by theliterature [1, 4, 8, 12, 16, 19, 22, 24, 28]. Never-theless, we think that our management is justi-fiable. PROM occuring before 28 weeks of ges-tation generally leads to fetal loss. However, ourmanagement led to a neonatal mortality rate ofonly 12% with a rate of 29% for HMD, 25%of neonatal infection and 33% of birth weightunder 1000 g. We had no latency period of less

than two days. Moreover, when PROM occuredafter 34 weeks of pregnancy, our conservativemanagement avoided prematurity in 38% of theneonates with no neonatal death and no HMD.Only one case (1%) of neonatal infection wasthe resulting risk.When compared with the literature, our rate ofchorioamnionitis seems rather high: 18% before37 weeks versus 12% [11], 5.2% [38], 5.3% [6]and 27% before 35 weeks versus 16% [15], 27%[27], 18% [17], 25% [16]. However, when com-paring the neonatal outcome, which is the mostimportant criteria, our PROM management issubstantially more encouraging than the tradi-tional management (table V).

Abstract

The aim of the study is to evaluate an active conserv-ative management (tocolysis and antibiotics adminis-tration) in preterm premature rupture of the mem-branes (PROM), applied to 215 singleton pregnancies.Pregnancies are continuated until 37 weeks of gestationif the clinical and biological follow-up shows no riskfor the mother and the fetus. The neonatal results wereanalysed by statistical methods and were compared tothe outcome of a control group of premature neonates.Our results show that the outcome is mostly deter-mined by gestational age at membrane rupture. No

benefit nor risk was added when glucocorticoids wereadministrated. Clinical suspicion of chorioamnionitisincreases the risk of neonatal infection. A prolongedlatency period (> 7 days) does not increase the mater-nal or fetal infection risk. When birth happened before35 weeks and before 37 weeks, the premature neonateafter PROM has a lower incidence of hyaline mem-brane disease and neonatal death compared with thecontrol group. These results are in favor of an activeconservative management in PROM.

Keywords: Chorioamnionitis, glucocorticoid, hyaline membrane disease, latency period, neonatal death, neo-natal infection, premature rupture of fetal membranes.

J. Perinat. Med. 17 (1989)

Page 8: J. Perinat. Med. Preterm premature rupture of the

430 Theunissen et al, Neonatal outcome in PROM

Zusammenfassung

Neonatales Outcome in 215 Fällen bei vorzeitigem Bla-sensprung und aktivem „klassischen" ManagementDer vorzeitige Blasensprung bei Geburtsunreife ist einHauptproblem der Geburtshilfe. In unserer Abteilungführen wir eine Antibiose sowie eine Tokolyse mitRitodrin durch. Wenn aus geburtshilflicher Sicht Glu-kokortikoide gerechtfertigt erscheinen, werden diesezur Akzeleration der Lungenreifung eingesetzt. Wirwürden dieses Vorgehen als aktives konservatives bzw.klassisches Management bezeichnen. Der klinischeVerlauf sowie die Kontrolle der Laborparameter erlau-ben die Fortsetzung der Schwangerschaft ohne Risiko,welches meist durch eine Infektion droht, für Mutterund Fet. Mit Erreichen der 37. Woche wurden dieSchwangerschaften beendet. Über einen Zeitraum von10 Jahren wurde dieses Vorgehen bei 215 Einlings-schwangerschaften mit vorzeitigem Blasensprung undGeburtsunreife angewandt. Das neonatale Outcomewurde statistisch analysiert. Darüberhinaus haben wirdieses Kollektiv verglichen mit einer Kontrollgruppevon Frühgeborenen ohne vorzeitigen Blasensprung.

Die Ergebnisse zeigen, das das Outcome in erster Liniedurch das Gestationsalter zum Zeitpujkt des Blasen-sprung bedingt ist (Tabelle II). Die Gabe von Gluko-kortikoiden brachte keine Vorteile, erhöhte aber auchnicht das Risiko. Bei klinischem Verdacht auf eineChorioamnionitis wurde häufiger eine neonatale In-fektion bestätigt (Tabelle III). Eine längere Latenzzeit(> 7 Tage) erhöhte nicht das Risiko einer maternalenoder fetalen Infektion. Bei Geburt vor der 35. bzw.vor der 37. Woche hatten Frühgeborene nach vorzei-tigem Blasensprung seltener ein Atemnotsyndrom alsKinder der Kontrollgruppe. Auch die neonatale Sterb-lichkeit war geringer (Tabelle IV).Diese Ergebnisse haben ihren Stellenwert in den zahl-reichen und kontroversen Arbeiten zum vorzeitigenBlasensprung. Unser aktives „klassisches" Manage-ment stimmt nicht mit der heutigen Vorgehensweisebeim vorzeitigen Blasensprung überein. Dennoch sindunsere Ergebnisse hinsichtlich des neonatalen Outcomeim Literaturvergleich ermutigend (Tabelle V).

Schlüsselwörter: Atemnotsyndrom, Chorioamnionitis, Glukokortikoide, Latenzzeit, neonatale Infektion, neo-natale Sterblichkeit, vorzeitiger Blasensprung.

Resume

Rupture prematuree des membranes ovulaires: resultatneonatal dans 215 cas d'un traitement conservateur actifLa rupture prematuree des membranes ovulaires(RPM) est un probleme obstetrical majeur qui bene-ficie dans notre institution d'un traitement conserva-teur actif. Le traitement consiste en une antibiotherapieet en une tocolyse ä base de ritodrine ainsi que Pad-ministration de glucocortico'ides dans le but d'accelererla maturation pulmonaire, si Petat obstetrical en in-dique Putilite. Une surveillance clinique et biologiquepennet de prolonger la grossesse sans risques (princi-palement infectieux) pour la mere et le fetus. Une foisle terme de 37 semaines atteint, la grossesse est inter-rompue. Sur une periode de 10 ans ce traitement a eteapplique ä 215 grossesses monofcetales avec RPM. Lesresultats perinataux ont ete evalues par analyse statis-tique. Nous avons egalement compare le devenir neo-natal des nouveaux-nes prematures apres RPM ä ungroupe contröle de prematures.

Le resultat neonatal semble principalement determinepar Tage gestationnel au moment de la rupture (tableauII). Aucun benefice ni risque n'ont ete mis en evidencesuite ä Padministration de glucocorticoi'des. La suspi-cion clinique de chorioamniotite augmente le risqued'infection neonatale (tableau III). Une periode delatence prolongee (> 7 jours) n'augmente pas le risqueinfectieux maternel ou neonatal. Quand la naissancesurvient avant 35 semaines et avant 37 semaines, laprematurite apres RPM presente un taux de maladiedes membranes hyalines et de mortalite neonatale plusbas que celui du groupe contröle (tableau IV).Ces resultats s'inscrivent dans Pabondante et contra-dictoire litterature concernant la RPM. Notre traite-ment conservateur actif ne correspond pas ä Papprocheactuelle de la RPM, mais nos resultats neonatauxcompares a ceux de la litterature sont encourageants(tableau V).

Mots-cles: Choriamniotite, deces neonatal, glucocortico'ides, infection neonatale, maladie des membraneshyalines, periode de latence, rupture prematuree des membranes ovulaires.

References

[1] ANDREYKO JL, CP CHEN, AT SHENNAN, JE MIL-LIGAN: Results of conservative management ofpremature rupture of the membranes. Am J Ob-stet Gynecol 148 (1984) 600

[2] AUBRIOT FX, MC LAFAY, R TAURELLE: La ruptureprematuree des membranes. A propos de 169 ob-servations relevees ä la maternite de Phopital Bou-cicaut. J Gyn obst Biol Repr 12 (1983) 423

J. Perinat. Med. 17 (1989)

Page 9: J. Perinat. Med. Preterm premature rupture of the

Theunissen et al, Neonatal outcome in PROM 431

[3] BLACKMON LR, LS ALGER, C CRENSHAW, JR: Fe-tal and neonatal outcomes associated with pre-mature rupture of the membranes. Clin ObstetGynecol 29 (1986) 779

[4] BLANCO JD: Rupture of the membranes in pre-term gestation. Clin Obstet Gynecol 27 (1984) 60

[5] BOTTOMS SF, RA WELCH, IE ZADOR, RJ SOKOL:Clinical interpretation of ultrasound measure-ments in preterm pregnancies with premature rup-ture of the membranes. Obstet Gynecol 69 (1987)358

[6] BROEKHUIZEN FF, M GILMAN, PR HAMILTON:Amniocentesis for gram stain and culture in pre-term premature rupture of the membranes. ObstetGynecol 66 (1985) 316

[7] CAPELESS EL, PB MEAD: Management of pretermpremature rupture of membranes: Lack of a na-tional consensus. Am J Obstet Gynecol 157 (1987)11

[8] Cox, SM, ML WILLIAMS, KJ LEVENO: The naturalhistory of preterm ruptured membranes: What toexpect of expectant management. Obstet Gynecol71 (1988) 558

[9] CURET LB, AV RAO, RD ZACHMAN, JC MORRI-SON, G BURKETT, WK POOLE, C BAUER: Associ-ation between ruptured membranes, tocolytictherapy, and respiratory distress syndrome. Am JObstet Gynecol 148 (1984) 263

[10] DOUVAS SG, MJ BREWER, ML Me KAY, PGRHODES, JH KAHLSTORF, JC MORRISON: Treat-ment of premature rupture of the membranes. JReprod Med 29 (1984) 741

[11] DRUZIN ML, M TOTH, WJ LEDGER: Noninterven-tion in premature rupture of the amniotic mem-branes. Surg Gynecol Obstet 163 (1986) 5

[12] FERRELL RE: Management of preterm prematurerupture of membranes. J Florida MA 70 (1983)739

[13] GARITE TJ: Premature rupture of the membranes:The enigma of the obstetrician. Am J Obstet Gy-necol 151 (1985) 1001

[14] GONIK B, SF BOTTOMS, DB COTTON: Amnioticfluid volume as a risk factor in preterm prematurerupture of the membranes. Obstet Gynecol 65(1985) 456

[15] HAWRYLYSHYN P, P BERNSTEIN, JE MILLIGAN, S.SOLDIN, A POLLARD, B CHIR, FR PAPSIN: Pre-mature rupture of membranes: The role of C-reactive protein in the prediction of chorioamni-otitis. Am J Obstet Gynecol 147 (1983) 240

[16] HURWITZ A, A ADONI, Z PALTI, A MILWIDSKY:Is conservatives management of preterm ruptureof membranes justified? Int J Gynaecol Obstet 22(1984) 131

[17] ISMAIL MA, MJ ΖΓΝΑΜΑΝ, RI LOWENSOHN, AHMOAWAD: The significance of C-reactive proteinlevels in women with premature rupture of mem-branes. Am J Obstet Gynecol 151 (1985) 541

[18] JOHNSON JW, NH DAIKOKU: Prepartal rupture ofthe chorioamnion. Birth Defects 21 (1985) 73

[19] KOSSMANN JC, G MELLIER, B L SALLE: Conse-quences des ruptures prematurees des membranes

32 semaines de gestation et moins sur la mor-bidite et la mortalite neonatales. Ann Pediat 31(1984) 361

[20] MILLER JM; JG PASTOREK II: The microbiologyof premature rupture of the membranes. Clin Ob-stet Gynecol 29 (1986) 739

[21] MOBERG LJ, TJ GARITE, RK FREEMAN: Fetal heartrate patterns and fetal distress in pateints withpreterm premature rupture of membranes. ObstetGynecol 64 (1984) 60

[22] MONIF GR, R HUME JR, RC GOODLIN: Neonatalconsiderations in the management of prematurerupture of the fetal membranes. Obstet GynecolSurvey 41 (1986) 531

[23] MORALES WJ, MD DIEBEL, AJ LAZAR, D ZAD-ROZNY: The effect of antenatal dexamethasoneadministration on the prevention of respiratorydistress syndrome in preterm gestations with pre-mature rupture of membranes. Am J Obstet Gy-necol 154 (1986) 591

[24] NELSON LH, PJ MEIS, CG HATJIS, JM ERNEST, RDILLARD, HM SCHEY: Premature rupture of mem-branes: A prospective, randomized evaluation ofsteroids, latent phase, and expectant management.Obstet Gynecol 66 (1985) 55

[25] NIE NH, CH HULL, JG JENKINS, K STEINBREN-NERER, DH BENT: Statistical Package for the So-cial Sciences. McGraw-Hill, New York 1975

[26] NIMROD C, F VARELA-GITTTNGS, G MACHIN, DCAMPBELL D, R WESENBERG: The effect of veryprolonged membrane rupture on fetal develop-ment. Am J Gynecol 148 (1984) 540

[27] ROMEN Y, J GREENSPOON, R ARTAL: Clinical cho-rioamniotitis-analysis of the incubation period inpatients with premature rupture of membranes.Am J Perinat 2 (1985) 314

[28] RUDD EG: Premature rupture of the membranes:A review. J Reprod Med 30 (1985) 841

[29] SCHMIDT PL, ME SIMS, HT STRASSNER, RH PAUL,E MUELLER, D Me CART: Effect of antepartumglucocorticoid administration upon neonatal res-piratory distress syndrome and perinatal infec-tion. Am J Obstet Gynecol 148 (1984) 178

[30] SHAVER DC, JA SPINNATO, D WHYBREW, WKWILLIAMS, GD ANDERSON: Comparison of phos-pholipids in vaginal and amniocentesis specimensof patients with premature rupture of membranes.Am J Obstet Gynecol 156 (1987) 454

[31] SIMPSON GF, GM HARBERT: Use of -Methasonein management of preterm gestation with pre-mature rupture of membranes. Obstet Gynecol 66(1985) 168

[32] SPINNATO JA: Infrequency of pulmonary imma-turity in an indigent population with prematurerupture of the membranes. Obstet Gynecol 69(1987) 942

[33] SPINNATO JA, DC SHAVER, EM BRAY, J LIPSHITZ:Preterm premature rupture of the membranes

J. Perinat. Med. 17 (1989)

Page 10: J. Perinat. Med. Preterm premature rupture of the

432 Theunissen et al, Neonatal outcome in PROM

with fetal pulmonary maturity present: A pro-spective study. Obstet Gynecol 69 (1987) 196

[34] SPITZER M, A FLEISCHER, H SCHULMAN, G FAR-MAKIDES: Impact of perinatal asphyxia, mode ofdelivery, and duration of premature rupture ofmembranes on the incidence of the respiratorydistress syndrome. NY State J Med 86 (1986) 64

[35] TAMURA RK, RE SABBAGHA, R DEPP, N VAISRUB,SL DOOLEY, ML SOCOL: Diminished growth infetuses born preterm after spontaneous labor orrupture of membranes. Am J Obstet Gynecol 148(1984) 1105

[36] TAYLOR J, TJ GARITE: Premature rupture of mem-branes before fetal viability. Obstet Gynecol 64(1984) 615

[37] VAN DONGEN PW, J ANTONISSEN, HW JONGSMA,JM SPORKEN, PR HEIN: Lethal lung hypoplasiain infants after prolonged rupture of membranes.Eur J Obstet Gynecol Reprod Biol 25 (1987) 287

[38] VAN DORSTEN JP, EO HORGER, MC MILLER: Pre-term rupture of the membranes: Combinationtherapy. Am J Obstet Gynecol 153 (1985) 147

[39] VINTZILEOS AM, WA CAMPBELL, D NOCHIMSON,ME CONNOLLY, MM FUENFER, GJ HOEHN: Thefetal biophysical profile in patients with prema-ture rupture of the membranes: An early predictorof fetal infection. Am J Obstet Gynecol 152 (1985)510

[40] VINTZILEOS AM, WA CAMPBELL, D NOCHIMSON,PJ WEINBAUM: Fetal breathing as a predictor ofinfection in premature rupture of the membranes.Obstet Gynecol 67 (1986) 813

Received July 1, 1989. Accepted August 31, 1989.

Michel van LierdeUnite d'ObstetriqueCliniques Universitaires Sl LucAv. Hippocrate 10B-1200 BrusselsBelgium

J. Perinat. Med. 17 (1989)