PERINATAL · 2015. 2. 11. · PERINATAL JOURNAL Volume 13 / Issue 3 / September 2005 The Official...

1993

Volume 13 / Issue 3 / 2005

PERINATAL

The Official Publication of Turkish Perinatology Society

JOURNAL

ISSN 1300-5251

•TÜRK

PER‹N

ATOLOJ‹ DERNE⁄‹•

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PERINATOLOGY

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PERINATAL JOURNALVolume 13 / Issue 3 / September 2005

The Official Publication of Perinatal Medicine Foundation

On behalf of the Perinatal Medicine Foundation: Murat Yayla

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ISSN 1300-5251

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— Standard journal article: Hammerman C, Bin-Nun A, Kaplan M.Managing the patent ductus arteriosus in the premature neonate: a newlook at what we thought we knew. Semin Perinatol 2012;36:130-8.

— Article published in an only electronic journal: Lee J, Romero R,Xu Y, Kim JS, Topping V, Yoo W, et al. A signature of maternal anti-fetalrejection in spontaneous preterm birth: chronic chorioamnionitis, anti-human leukocyte antigen antibodies, and C4d. PLoS ONE 2011;6:e16806.doi:10.1371/ journal.pone.0011846.

— Book: Jones KL. Practical perinatology. New York: Springer; 1990.p. 112-9.

— Chapter in a book: Sibai BM, Frangieh AY. Eclampsia. In: GleicherN, editors. Principles and practice of medical therapy in pregnancy. 3rd ed.New York: Appleton&Lange; 1998. p. 1022-7.

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Perinatal JournalVolume 13 / Issue 3 / September 2005

Contents

Role of Doctors, Midwives and Nurses in Oxytocin Administration Nurdan Demirci, Özlem Gürkan, Hediye Arslan, Zübeyde Ekfli

Frequency of Genetic Thrombophilia in Severe Intrauterine Growth Restriction

Rag›p Atakan Al, Serdar Yalvaç, Esmen Öztürko¤lu, Erol Akkök, Ömer Kandemir, ‹smail Dölen

Maternal Serum Concentrations of Metabolites of Nitric Oxide in Preeclampsia

Levent Tütüncü, Emine Özdemir, Ercüment Müngen, Ali Rüfltü Ergür,Yusuf Z. Yergök

Conservative Managemenet of Twin Pregnancy After Delivery ofOne Fetus at the Second Trimester of the Pregnancy

Cem Dane, Murat K›ray, Salih Dural, Mukadder Tayhan, Ahmet Aliosmano¤lu, Murat Yayla

Relationship of Early Diastolic Notch in Uterine Artery Doppler Measurements With Pregnancy Complications in Low Risk Pregnancies

Faik Gürkan Yaz›c›, Ekrem Tok, S›tk› Gülhan, Devrim Ertunç, Gülay Özdemir, Saffet Dilek

Retrospective Analysis of Polyhydramnios CasesAhmet Kale, Nurten Akdeniz, Mahmut Erdemo¤lu, Ahmet Yal›nkaya, Murat Yayla

A Case Report of Meconium Ileus-Peritonitis with a PrenatalDiagnosis of Sacro-Coccygeal Teratoma

Baflak Baksu, ‹nci Davas, Jale Özgül, Figen Ezen, Alper Özel, Gülden Yenice, Mehmet Yalç›n

Patau Syndrome (Trisomy 13): Autopsy CaseNihal K›l›nç, Bülent Demir, Diclehan Orhan, Murat Yayla

Thromboembolic Cases in the Pregnancy and Pulnomery Embolism after Cesarean: Case Presentation

Nimet fieno¤lu, Hafize Öksüz, Beyaz›t Zencirci, Meral Ezberci, K›ran Gürkan, Okur Nazan

17 Week Non-Communicating Rudimenter Uterine Horn Pregnancy and Uterine Rupture: Case Report

Serkan Kahyao¤lu, ‹nci Turgay, Oktay Kaymak, fienol Kalyoncu, Leyla Mollamahmuto¤lu

Research Articles

Case Reports

129

138

142

148

152

158

163

169

173

179

Perinatal Journal • Vol: 13, Issue: 3/September 2005 129

Abstract

Objective: In order to evaluate oxytocin administration and determine the difficulties encountered by doctors, nurses and mid-wives.

Methods: 53 midwives and nurses and 25 doctors who accepted to participate were included in the study. Questions about thedifficulties of oxytocin administration and solution suggestions for these difficulties were adressed and acquired data was eval-uated quantatively and qualitatively.

Findings: 84.9% of midwives and nurses 76% of doctors have experienced difficulties during oxytocin administration. There aredifficulties of oxytocin administration because of uncooperative patients, lack systematic of monitoring, sufficient equipmentand an oxytocin protocol.

Result: Difficulties encountered during oxytocin administration can be decreased by using oxytocin protocols.

Keywords: Oxytocine usage, role of health professional.

Oksitosin uygulamalar›nda hekim, ebe ve hemflirelerin rolü

Amaç: Do¤umhanelerde çal›flan hekim, ebe ve hemflirelerin oksitosin uygulamalar›n› de¤erlendirmek ve uygulama s›ras›nda kar-fl›laflt›klar› güçlükleri belirlemek amac›yla tan›mlay›c› olarak yap›lm›flt›r.

Yöntem: Hastanelerin do¤umhanelerinde çal›flan ve araflt›rmaya kat›lmay› kabul eden 53 ebe ve hemflire ile 25 hekim çal›flmakapsam›na al›nm›flt›r. Ebe, hemflire ve hekimlere oksitosin kullan›m›, kullan›m s›ras›nda karfl›laflt›klar› sorunlar ve çözüm önerileriile ilgili sorular sorulmufl, elde edilen veriler yüzdelik ve kalitatif olarak de¤erlendirilmifltir

Bulgular: Oksitosin uygulamas› s›ras›nda ebe ve hemflirelerin %84.9’u, hekimlerin %76’s› güçlük yaflamaktad›r. Yaflanan güçlük-ler; hastalar›n tedaviye uyumsuzlu¤u, takipteki aksamalar, malzeme eksikli¤i ve oksitosin protokolünün bulunmamas›ndan kay-naklanmaktad›r.

Sonuç: Oksitosin uygulamas› s›ras›nda karfl›lafl›lan güçlükler, oksitosin protokolü kullan›m› ile azalt›labilir niteliktedir.

Anahtar Sözcükler: Oksitosin kullan›m›, sa¤l›k personelinin rolü.

Role of Doctors, Midwives and Nurses inOxytocin Administration

Nurdan Demirci, Özlem Gürkan, Hediye Arslan, Zübeyde Ekfli

School of Nursing, Marmara University, ‹stanbul

Correspondence: Özlem Can, Marmara Üniversitesi Haydarpafla Kampüsü, Hemflirelik Yüksekokulu, T›bbiye Cad. No: 49 Üsküdar 81326 ‹stan-bul, e-mail: [email protected]

Introduction

Synthetic oxytocin which is a medicine

approved by FDA (Food and Drug Administration)

is commonly used in our country and the world.

Usage frequency of oxytocin which is used withthe aim of preventing parturition induction, thera-peutic aborts, postpartum bleeding and providingpostpartum lactation is increasingly raising nowa-days.1-7

While it is declared than oxytocin was used in708.151 parturitions (18.4% of all parturitions) inUnited States this rate was stated as 20% in 2000.1,8

Although there is no data about oxycotin usagein obstetric clinics in our country, it is known thatit is commonly used for induction of parturition. Incases pregnancy is required to be ended (due topregnancy-based hypertension, early membranerupture, chorioamnionitis, abnormal pregnancytests (anencephaly, chromosome anomalies etc),intrauterine growth retardation, Rh incompatibility,over termination, diabetes in mother, kidney dis-ease, chronic obstructive lung diseases and heartdisease) oxytocin usage is recommended in apregnant in/over its termination in order to startparturition pains or to increase insufficientpains.4,9,11,12,17

Attentive evaluation of patient and fetus beforeusage and attentive monitoring of mother andfetus during usage are essential in order to preventpossible complications. Inattentive usage of oxy-tocin may cause damage in mother and baby.2,4,11,12

Start of treatment should be decided after pre-conditions required for the application are provid-ed. In recent years there are 2 treatment protocolsrecognized by ACOG (American College ofObstetricians and Gynecologists) relating to initialand improved doses of oxytocin. ACOG explainedlow and high dose treatment protocols inNovember 1999 bulletin (Table 1).8 ACOG recom-mends oxytocin treatment to be prepared byadding 10 units of oxytocin in 1000cc isotonic liq-uid. oxytocin has some adverse effects like hyper-stimulation (regardless of there is disruption infetal heart rate), ablatio placentae, disruption in

uterus blood stream, rapid parturition activity,uterus rupture, hyponatremia and postpartumbleeding which threat the health of mother andsome other like fetal hypoxia, hiperbilirubinemia,fetal trauma and fetal death as a result of rapid par-turition activity which affect the health of fetus. Inaddition, oxytocin may lead to liquid intoxicationby making a weak antidiuretic hormone effect.Symptoms of liquid intoxication are lethargy,headache and defect of eyesight. A severe liquidintoxication may lead to death due to convulsions,coma and cerebral edema.1,3-5,7,8,10,13,16

With the aim of preventing liquid intoxicationACOG has emphasized that oxytocin should betaken in isotonic solution.1

In order to prevent complications which mayaffect both mother’s and fetus’ health during oxy-tocin administration doctors, midwives and nursesshould behave attentively.

Midwives and nurses are responsible frompreparation of IV (Intra Venous) solution, evalua-tion of patient before and during the application interms of counter indications, and evaluation ofresponses of uterus and fetus to treatment.11-15

The purpose of our study is to determine theroles of doctors, midwives and nurses working instate and SSK hospitals placed in Istanbul and inwhich number of parturitions are so high in andthe difficulties they encountered during oxytocinadministration.

Methods7 research and application hospitals dependent

on Ministry of Health and monthly parturition

Demirci N et al., Role of Doctors, Midwives and Nurses in Oxytocin Administration130

Treatment Initial dose Agreed increase in dose Dose increase intervals

mÜ/dk (mÜ/dk) (dk)

Low dose 0.5-1 1 30-40

1-2 2 15

High dose ~6 ~6 15

6 6*, 3,1 20-40

Table 1. Induction of parturition with oxytocin: low and high dose treatment protocol (formof oxytocin administration) (recommended by ACOG).

*: This amount is decreased to 3 mU/min in case of hyperstimulation and to 1 mU/min if hyperstimulation repast.


number of which is over 100 were taken within thecontext of the study. The research was performedin obstetric clinics of the hospitals descriptivelybetween 1 and 15 January 2004.

All midwives, nurses and doctors working inobstetric units of the hospitals constituted the uni-verse of the research. 95 midwives and nurses and55 doctors changing with shifts or rotations (whowere in rotation during the research) serve inobstetric units of the hospitals. 53 midviwes-nurs-es and 25 doctors were taken in sampling group ofthe research.

Data were obtained by using question formsprepared by the researcher differently for mid-wives, nurses and doctors.

In question for prepared for midwives, nurses;questions including what they do before applyingoxytocin treatment, their roles during the applica-tion of treatment, effects of the treatment, prob-lems encountered during oxytocin application andsolution recommendations for these problemswere present.

In question form prepared for doctors their cri-teria to start oxytocin treatment, problems theyencountered about oxytocin administration andsolution recommendations, their expectations frommidwives and nurses during oxytocin administra-tion.

Question forms prepared by midwives, nursesand doctors were filled by the individuals throughmutual interview techniques.

Obtained data were evaluated as percentageand qualitative.

ResultsIt was determined that different oxytocin appli-

cations are performed in hospitals we have includ-ed within the context of the research and any ofwhich does not have a oxytocin treatment proto-col written and approved by the institution.

20% among 25 doctors included within thestudy was specialist and 80% of which was gener-al practitioner. When we examine the workingperiods of doctors in obstetric clinics it was 31.9 ±37.1 month in average.

11.3% among 53 midwives and nurses withinthe study was nurse and 8.1% was midwife and7.5% was officer midwife.

64.2% of midwives and nurses graduated fromtwo-year degree and 26.4% from health vocationalhigh school and 9.4% has graduate degree andtheir working period was 6.6 ± 6.6 year in average.

All doctors have stated that they start oxytocintreatment in order to activate obstetric pains and incase parturition activity is definitely required to bestarted (intrauterine growth retardation, intrauter-ine fetal death, early membrane rupture, oligohy-droamnios etc.) if condition of fetus is good andBishop score is appropriate (Table 2).

When we ask about adverse effects of oxytocin94.3% of midwives and nurses answered as dis-ruption in fetal heart rate, 73.6% answered asuterus hyperstimulation, 47.2% answered as nau-sea-vomiting, 39.6% answered as fetal- maternaltachycardia and 1.9% answered as decrease inurine amount (Table 3).

On the other hand it was determined that 16.1%among midwives and nurses have evaluated someadverse effects not resulted from oxytocin as ifthey resulted from oxytocin.

When distribution among attempts of midwivesand nurses before oxytocin application, it was

Criteria to start oxytocin treatment

• In order to activate insufficient pains in parturition if the condition of fetus is

normal and Bishop score is at least 5

• In case parturition activity is required to be started

• To accelerate parturition activity in normal progress

• Atonia bleedings

n* %

25 100

25 100

4 16

4 16

Table 2. Distribution of criteria of doctors to start oxytocin treatment.

*: n is multiplied since multiple answer was given

determined that such a high percentage like 86.8%declared that patient is informed, 71.7% declaredthat vital findings are checked, 77.4% declared thatNST application is performed (not stating a peri-od), 67.9% declared that FHS (fetal heart sound) ischecked, and such a low percentage like 26.4%declared that Leopold maneuvers are applied(Table 4).

When the follow-ups performed by midwivesand nurses and their frequencies are examined inTable 5 it was determined that blood pressure of

patient is followed-up regularly in a percentage of54.7%, regular vaginal examination is performed in43.3%, regular FHS check is performed in 47.2%


Adverse effects of oxytocin

• Disruption in fetal heart rate

• Hyperstimulatflon of uterus

• Nausea / vomiting

• Tachycardia (fetal / maternal)

• Headache

• Defect cardiac rate

• Respiration defect

• Decrease in urine amount

• Confusion

• Cases which are not adverse effects of oxytocin

n* %

50 94.3

39 73.6

25 47.2

21 39.6

4 7.5

4 7.5

2 3.8

1 1.9

1 1.9

8 16.1

Table 3. Distribution of views of midwives and nurses aboutadverse effects of oxytocin.


Applications n (53) %

Whether patient is informed • Informed 46 86.8• Not informed 7 13.2

Vital symptoms • Checked 38 71.7• Not checked 15 28.3

NST (Non Stress Test)• Applied 41 77.4• Not applied 12 22.6

FHS evaluation • Applied 36 67.9• Not applied 17 32.1

Vaginal examination • Applied 31 58.5• Not applied 22 41.5

Anamnesis check • Checked 25 47.2• Not checked 28 52.8

Leopold examination • Applied 14 26.4• Not applied 39 73.6

Table 4. Distribution of initiatives of midwives and nursesbefore oxytocin application.

Applications n (53) %

Follow-up with fetal monitoring • Performed regularly (continually) 20 37.7

• Performed irregularly 14 26.4

• No answer 15 28.3

• Not performed 4 7.5

FHS follow-up• Regularly (in every 15 minute) 25 47.2

• Not regularly 17 32.1


Vaginal examination• Regularly (in every one hour) 23 43.3



• Not examined 3 5.7

Follow-up contraction • Regularly (in every 15 minute) 13 24.5



• Not followed-up 4 7.5

Amniotic fluid amount, color and density • Regularly (in every one hour) 18 34




Blood pressure of patient • Regularly (in every half an hour) 29 54.7



Pulse rate of patient • Regularly (in every half an hour) 17 32.1



Respiration of patient • Regularly (in every half an hour) 12 22.6



Food inlet and vomiting • Regularly (in every one hour) 1 1.9


• Regular in patients with preeclampsia 8 15.1


• Not examined 9 17

Control of infusion dose • Regularly (in every half an hour) 21 39.6


Control of any obstruction in set if exist • Regularly (in every half an hour) 18 34


Table 5. Distribution of follow-ups and frequency of these follow-upsperformed by midwives and nurse during oxycotin application.

*: Sources we have referred for follow-up frequencies (1,4,5,9,12,14,15,16,17).

(in every hour in latent phase, in every 15-30 min-utes in active phase), and the color and density ofamniotic fluid is evaluated regularly in 34%.

Moreover, it is determined that pulse rate ofpatient in 47.2%, respiration in 24.5%, food inletand vomiting in 22.6%, control of infusion dose in60.4%, check of obstruction in set in 66.1% are fol-lowed up not regularly.

When we examined difficulties encountered bymidwives, nurses and doctors relating to oxytocinapplication (Table 6); 56.6% percent of midwivesand nurses and 48% of doctors stated that theyencounter difficulty due to incompatibility ofpatient with treatment (patient may try to removeprenatal applied oxytocin by reason of pain, speedup of flow for medicine application to be com-pleted early, rejection of patient to treatment etc.),and the rate of difficulties encountered resultedfrom trouble in follow-ups because of insufficientnumber of midwives and nurses are 39.6% in mid-wives and nurse and 28% in doctors.

It was also determined that insufficient numberof fetal monitor was indicated as a reason by sucha high percentage of doctors like 56% and by18.9% of midwives and nurses.

Doctors, and midwives and nurses encounterdifficulty due to the lack of oxytocin treatment pro-tocol in such a low rates in respectively 12% and11.3%.

When we examined the recommendations ofmidwives, nurses and doctors with the aim ofremoving difficulties encountered about oxytocinapplication, it was determined that 28midwives/nurses and 2 doctors have no recom-mendation. When recommendations of midwives,

nurses and doctors who made a recommendation52% of midwives and nurses and 56.5% of doctorsstated that the difficulties can be removed byincreasing the number of materials (monitor, dose-flow, pump etc.) and through preparation of anoxytocin treatment protocol (8% of midwives andnurses and 8.6% of doctors) (Table 7 and 8).

While 52% of midwives and nurses think thatthe difficulties can be decreased by follow-up ofpregnant women in pain clinic more regularly,95.6% of doctors stated that the difficulties can beremoved by follow up of pregnant women in painclinic by midwives and nurses more regularly and17.3% stated difficulties can be removed byincreasing the number of midwives and nurses towork effectively in obstetric clinics.

When we examined the expectations of mid-wives and nurses from doctors relating to oxytocinapplication; 45.4% stated that doctors should beattentive and not behave impatiently while select-ing patients, 27.2% stated preparation of oxytocintreatment protocol and performing dose arrange-ments by using this treatment protocol and 18%stated that doctors should write a formal request. Itwas also stated that 24 nurses among 53 do nothave any expectation (Table 9).

While 39% of doctors expected from midwivesand nurses to follow-up dropping speed andpatients regularly, only 9% stated that midwivesand nurses do not have enough information aboutoxytocin treatment (Table 10).

DiscussionDoctors, midwives and nurses should firstly

evaluate the patient while using oxytocin and


Problems

• Incompatibility of patients to treatment

• Troubles in follow-ups due to insufficient number of midwives and nurses

• Insufficiency in fetal monitor

• Communication gap between midwives and nurses and doctors

• Lack of oxytocin treatment protocol

• Not any problem encountered

Midwives and nurses

n* (53) %

30 56.6

21 39.6

10 18.9

11 20.8

6 11.3

8 15.1

Doctors

n* (25) %

12 48

7 28

14 56

5 20

3 12

6 24

Table 6. Distribution of difficulties encountered by midwives and nurses and doctors.


should inform patient about effects and adverse

effects of the treatment.7

Before the application Bishop scoring is

required to be evaluated and obtained value

should be at least 4, fetal lung maturation should

be ensured, pregnancy week should be appropri-

ate, situation of mother should be stable, size and

location of fetus should be appropriate.2,4 If Bishop

score is less than 4, possibility of failure in induc-tion is higher.4,7

Sometimes oxytocin treatment may be startedregardless of fetal maturity in situation whichthreat mother’s life.2,7

When we examined criteria of doctors to startoxytocin treatment in our research; it was deter-mined that all doctors use oxytocin in order to acti-vate insufficient pains in the parturition when par-turition activity is definitely required to be startedand Bishop score is 5 and more in accordance withthe literature.7

However another usage we obtained in ourstudy and which is not appropriate with the litera-ture is using oxytocin in order to gain time byaccelerating a parturition activity in its normalprogress. 16% of doctors use oxytocin with the aimof accelerating a parturition activity in its normalprogress. It can be considered that this usage isresulted from excess number of patients in obstet-ric clinics and the aim of preventing patient accu-mulation however it is not a desirable method.

Oxytocin has some adverse effects both interms of mother and baby.7 Midwives and nursesare considerably important in terms of beinginformed about adverse effects of oxytocin andearly notification of adverse effects.9 It should beremembered that the person who follow-up moth-er and fetus closely and who notice differences tooccur is midwives and nurses.

It was determined in our study that a big major-ity of midwives and nurses are aware of commonadverse effects of oxytocin like defect in fetal heartspeed and uterus hyperstimulation but not awarethe adverse effect of liquid intoxication (decrease


Recommendations

• Increase in the nube rof materials (monitor, dose-

flow, pump etc.) (monitör, doziflow, pumb v.b )

• More regular follow-up of patients

• Attention of doctors in treatment

• Development of a protocol

n* (25) %

13 52

13 52

8 32

2 8

Table 7. Recommendations of midwives and nurses relatingto difficulties encountered in oxytocin application.

*: n is multiplied since multiple answer was given, only those who has a recommendation(n=25) was evaluated.

Recommendations

• Careful follow-up of oxytocin dropping speed

• Regular follow-up of patient applied oxytocin

treatment

• Attentive follow-up whether or not vessel way

is open

• Provision of fetal monitoring and capacity of

interpreting NST

• Follow-up of complications to appear during

oxytocin application and informing patient

about them

• Ensuring midwives and nurses have sufficient

information about oxytocin treatment

n* (23) %

9 39

9 39

5 21.7

4 17.3

4 17.3

2 9

Table 8. Recommendations of doctors relating to difficultiesencountered in oxytocin application.


Expectations

• Doctors should be attentive while selecting

patients and should not behave impatiently

• Development of an oxytocin treatment pro-

tocol and performing dose arrangement by

using this protocol

• Writing order

• Doctors should not leave oxytocin application

time to late hours as far as possible

n* (22) %

10 45.4

6 27.2

4 18

3 13.6

Table 9. Expectations of midwives and nurses from doctorsExpectations.


Expectations

• Doctors should be attentive while selecting

patients and should not behave impatiently

• Development of an oxytocin treatment pro-

tocol and performing dose arrangement by

using this protocol

• Writing order

• Doctors should not leave oxytocin application

time to late hours as far as possible

n* (22) %

10 45.4

6 27.2

4 18

3 13.6

Table 10. Expectation of doctors from midwives and nurses.


in urine amount, headache and defect I heart rateetc.) which is rarely seen. It can be considered thatinformation which midwives and nurses arecaused by their earlier experiences.12

Midwives and nurses should make some expla-nations about the purpose, reason, of oxytocintreatment, problems which may appear during thetreatment and some warnings the patient shouldgive attention during the treatment in order toensure the patient and her family to comply withthe treatment before the application.11,12 Most ofmidwives and nurses have declared they givesome information for patients but did not explaincontext of information.

Evaluation of mother and baby by midwivesand nurses is so important in order to learn exist-ing problems and discover risky situations. Vaginaland abdominal evaluation of pregnant womentaken anamnesis should be fulfilled. Position andpresentation of the fetus should be evaluated withLeopold maneuvers abdominally applied. Vitalsymptoms of pregnant woman should be recordedand fetus heart speed should be listened. If thereis a counter indicated situation to start oxytocin adoctor should be notified.4,11,12

In the study performed by Goetzl et al it wasdetermined that patients who experienced uterusrupture before are more possible to experienceuterus hyperstimulation. For this reason oxytocinshould not be applied or applied with an attentivefollow-up in a patient who has a rupture history.13

In our study it was determined that a big major-ity of midwives and nurses check vital symptomsof patients before the treatment and evaluate thesituation of baby with fetal monitor.4,7,11,12,17

However, the rates of midwives and nurses whoevaluate situs and habitus of the baby by applyingvaginal examination, anamnesis check andLeopold maneuvers are low. We can say that theserates are such low since midwives and nurses arenot given a responsibility and everything is underresponsibility of doctors.

Fetal heart speed and contractions are continu-ously followed-up with electronic fetal monitorduring the regular oxytocin application and in caseof divergence from normal speed of fetal heartinfusion should be urgently turned off.4,7,11,12,17

The rate of follow-up with fetal monitor isfounded as low in our research due to the insuffi-cient number of fetal monitor and midwives, nurs-es and doctors also stated fetal monitor shortfall asa problem.

In this case result from insufficient fetal moni-tors midwives and nurses may notice complica-tions to appear in advance by frequently follow-ing-up FHS with manual Doppler or fetoskope andapplying contraction check in every 10 minutesaccording to the stage of travail. However, it can-not be said in our study that FHS follow-ups areperformed in phases determined in the literature(in every hour in latent phase and in every 15-30minutes in active phase) and regularly.4,11,12,16

Although midwives and nurses mostly knowdefect in heart speed and hyperstimulation asadverse effects of oxytocin it is thought provokingthat regular follow-up rates are low. Lowness ofregular FHS and contraction follow-up rates maybe related with the situation in some clinics wherethis responsibility is conferred to doctor and withinsufficient number of midwives and nurses.

The earliest forerunner of liquid intoxication,uteri rupture and ablatio placentae to happen dur-ing oxytocin application is defect in woman’s vitalfindings and in FHS and decrease in urine outlet.For this reason, nurses are required to performthese follow-ups with regular intervals. Moreoveranother early symptom of liquid intoxication isdefect in heart rate and heart of the patient shouldbe followed-up regularly.4,9,11,12,14,15

Even though more than half of midwives andnurses in our study stated that they perform regu-lar blood pressure check, it was determined thatthey do not perform pulse check regularly in ahigh percentage and half of midwives and nursesnever perform respiration check. However, bloodpressure, pulse and respiration checks should beregularly performed.

It was also determined that follow up of foodinlet and vomiting is almost never performed reg-ularly in normal pregnant women. This situationmay result from that midwives and nurses do notknow liquid intoxication as an adverse affect tohappen as a result of oxytocin usage and there arenot present easily used scaled cups in toilets.


The amount, color and density of amniotic fluidshould be checked and recorded.4,9,11,12,16

Oxytocin oscillates in human body in a rhyth-mic way by its nature.6 In order to ensure IVapplied oxytocin dose flows in a proper amount itshould be regularly followed-up whether there isany obstruction or excess flow in the set. Excessflown oxytocin leads to uteri hyperstimulation anduterus rupture insufficient flow of oxytocin doseprevents expected effect to happen.9,11,12,16

It was determined in our study that midwivesand nurses do not regularly check drop numbersobstructions in the set. Just like other follow-upsdefects in this follow-up may be caused by insuffi-cient number of nurses.

Patients who take oxytocin treatment should beregularly followed-up with electronic fetal monitorand infusion pumps should be used for oxytocindose to be flown in proper amounts.4,6,9,12,17 This jus-tification can more easily explain why doctorsencounter problems mostly caused by insufficientfetal monitor during oxytocin administration.Doctors, midwives and nurses have the commonview that this difficulty can be removed by increas-ing the number of materials.

While doctors encounter problems mostly dueto insufficient fetal monitor, midwives and nursesare in difficulty due to incompatibility of patientswith the treatment (patient or her relatives may tryto remove prenatal applied oxytocin by reason ofpain, and speed up of flow for medicine applica-tion to be completed early). While most midwivesand nurses in our study state that they informpatients before treatment, incompatibility ofpatients with the treatment indicates that providedinformation is insufficient.

While doctors recommend more regular follow-up of patients by midwives and nurses in order toremove problems encountered in oxytocin admin-istration, midwives and nurses recommend in asimilar way that doctors should follow up patientsmore regularly. This situation can be explained asthere is a confusion relating to responsibility allo-cation between doctors and nurses during the fol-low-ups. If there were protocols in obstetric clinicswhich clearly indicate responsibilities of both doc-tors and midwives and nurses during oxytocinadministration this confusion would be rarely

encountered. However in our study only a smallnumber of doctors and nurses have the view thatproblems can be diminished with the presence ofa oxytocin treatment protocol.

Majority of the doctors expect from midwivesand nurses to follow-up patients and droppingspeed of oxytocin. As we determined in our study,problems resulted from irregular follow-up of oxy-tocin infusion speed and patients by midwives andnurses may lead doctors to state such an expecta-tion.

On the other hand, midwives and nurses statedthat they expect from the doctors to pay attentionwhile selecting patients and not to behave impa-tiently.

In conclusion, it was determine din our studythat some problems are experienced relating tooxytocin usage, and these problems by theirnature can be prevented through preparation of aoxytocin treatment and follow-up protocol, mater-ial provision and training of patients. Oxytocintreatment and follow-up protocol should be innature which clearly state how and in which dosesthe medicine will be used, how much droppingapplication should be started with, follow-ups andfrequency of follow-ups required to be performedby midwives/nurses during the medicine applica-tion, emergency cases to be encountered duringthe medicine application and the roles of doctorsmidwives/nurses during the emergency cases.

Doctors, midwives and nurses should be incooperation and the roles of each in the applica-tion should be determined in while preparing andapplying a treatment and follow-up protocol.Institutions should remember that material defi-ciency in obstetric clinics may cause vital resultsand should attempt for provision of deficient mate-rials. In addition, information should be providedfor health personnel in hospitals relating to patienttraining methods.5

References

1. Ruchala PL, Metheny N, Essenpreis H, Borcherding K. Cur-rent practice in oxytocin dilution and fluid administrationfor induction of labor. JOGNN 2002; 31: 545-50.

2. Shyken JM, Petrie RH. The use of oxytocin. Clinics inPerinatology 1995; 22(4): 907-31.

3. Kayaalp O. Rasyonel Tedavi Yönünden T›bbi Farmakoloji,3. Cilt. Ankara, Feryal Matbaac›l›k, 1990.


4. Nichols F, Zwelling E. Maternal-Newborn Nursing TheoryAnd Practice. Phiadelphia, Saunders Company, 1997.

5. Martin LL, Reeder SJ. Essentials Of Maternity Nursing:Family-Centered Care. Phiadelphia, Lippincott Company,1991.

6. Willcourt RJ, Pager D, Wendel J, Hale RW. Induction oflabor with pulsatile oxytocin by a computer-controlledpump. Am J Obstet Gynecol 1994; 170(2): 603-8.

7. Royal Collage of Obstetrians and Gynaecologist. Inductionof labor. GUIDELINE. RCOG Press. London. (Guideline No:9), 2001 Jun., 78 pages.

8. Stubbs TM. Oxytocin for labor induction. Clinical Obstetricsand Gynecology 2000; 43(3): 489-94.

9. May KA, Mahlmeister L R. Comprehensive Maternity Nur-sing. Phiadelphia, Lippincott Company, 1990.

10. Gagnon AJ, Waghorn K. One-to-one nurse labor support ofnulliparous women stimulated with oxytocin. JOGNN 1999;28(4): 371-6.

11. Mccarthy MC, Mullee M. Oxytocin induction augmentationof labor. In: Gulanick M, Gradishar D, Puzas M K (Ed).Obstetric And Gynecologic Nursing. Albany, Delmar Publis-hers; 1994.

12. Simpson KR. Creehan PA. Perinatal Nursing. Philadelphia,Lippincott Company, 1994.

13. Goetzl L, Shipp TD, Cohen A, Zelop CM, Repke JT, Lieber-man E. Oxytocin dose and the risk of uterine rupture in trialof labor after ceserean. Obstet Gynecol 2001; 97(3): 381-4.

14. Clark AL, Affonso D. Childbearing: a Nursing PerspectiveEdition 2. Philadelphia, F.F. Davis Company, 1996.

15. Ladewing PW, London ML, Olds SB. Essentials of MaternalNewborn Nursing. California, A division of the benjamin /cummings publishing company, 1990.

16. Brodsky PL, Pelzar EM. Rationale for the revision of oxy-tocin administration protocols. JOGNN 1991; 20(6): 440-4.

17. Royal Collage of Obstetrians and Gynaecologist. The use ofelectronic fetal monitoring. GUIDELINE. RCOG Press. Lon-don. (Guideline No:8), 2001 May, 136 pages.


Abstract

Objective: To investigate the frequency of genetic thrombophilia in pregnancy complicated with severe intrauterin growthrestriction in which absent or reversed end-diastolic blood flow were detected.

Methods: We presented 17 cases with diagnosed as severe intrauterine growth restriction with absent or reversed end-diastolicblood flow and the test result of genetic thrombophilia (activated protein C resistance, protein C, free protein S antigen) wereavailable.

Results: Genetic thrombophilia was detected in 11 (%64.7) cases. In three cases (%17.6), two factor were estabilished. Theseratios were higher than the incidence for the normal population.

Conclusion: It seems that the frequency of genetic thrombophilia was increased in severe intrauterine growth restriction.

Keywords: Thrombophilia, intrauterine growth restriction, Doppler, pregnancy.

fiiddetli intrauterin geliflme yetersizli¤i olgular›nda genetik trombofili s›kl›¤›

Amaç: Umbilikal arterde diyastol sonu ak›m kayb› veya ters ak›m saptanan fliddetli intrauterin geliflme yetersizli¤i (IUGY) olgula-r›nda trombofili s›kl›¤›n› saptamak.

Yöntem: 2003-2005 tarihleri aras›nda umbilikal arterde diyastol sonu ak›m kayb› veya ters ak›m saptanan ve genetik trombofilitestleri yap›lm›fl (aktive protein C rezistans›, protein C aktivitesi, serbest protein S antijenitesi) fliddetli intrauterin geliflme yeter-sizli¤i saptanan 17 olgunun sonuçlar› incelendi.

Bulgular: Onbir vakada (%64.7) trombofili saptand›. Üç olguda (%17.6) iki faktör pozitifli¤i mevcuttu. Bu oranlar normal top-lum için bildirilen de¤erlerden yüksektir.

Sonuç: fiiddetli intrauterin geliflme yetersizli¤i saptanan olgularda daha yüksek oranda genetik trombofiliye rastlanabilir.

Anahtar Sözcükler: Trombofili, intrauterin geliflme yetersizli¤i, Doppler, gebelik.

Frequency of Genetic Thrombophilia in SevereIntrauterine Growth Restriction

Rag›p Atakan Al, Serdar Yalvaç, Esmen Öztürko¤lu, Erol Akkök, Ömer Kandemir, ‹smail Dölen

Ministry of Health Ankara Etlik Training and Research Hospital for Maternity and Gynecological Diseases, Ankara

Correspondence: Dr. Rag›p Atakan Al, Sa¤l›k Bakanl›¤›, Ankara Etlik Do¤umevi ve Kad›n Hastal›klar› E¤itim Araflt›rma Hastanesi, Ankarae-mail: [email protected]

Introduction

Genetic thrombophilia is used to define a

group of genetic hypercoagulability disorder that

can cause thrombosis. Factor V Leiden (FVL),

methylenetetrahydrofolate reductase, prothrombinG20210A mutations and protein C, protein S andantithrombin III deficiencies are commonly speci-fied from this group. Recent studies give rise tothought that there may a relationship between

Perinatal Journal • Vol: 13, Issue: 3/September 2005138

genetic thrombophilia and obstetric complica-tions.1 There are many retrospective and someprospective studies about the relationship betweengenetic thrombophilia and intrauterine growthrestriction in the literature. But these studies is aheterogenic group because methods selecting thepatient and number of patients; the results dis-agree with each other. Publications that examinethe relationship between intrauterine growthrestriction and genetic thrombophilia whose num-ber of case is relatively low give rise to thoughtthat genetic thrombophilia can be one of the rea-sons for intrauterine growth restriction.2-8 But thisrelationship is not observed in the larger series.9,10

Infants with low birth weight according topregnancy week form a heterogenic group. Somegroup of these infants is unable to develop for thereason of malnutrition reasoning from placentaldeficiency. Other group includes the healthyinfants structurally small and abnormal infants hav-ing fetal abnormality, chromosome aberrations ortransmitted the intrauterine disease.

It is known that more thrombotic processes areseen more for the cases showing preeclampsia andintrauterine growth restriction than the normalinfants in the placenta studies.11-13 Although thereare contrary studies, it is thought that geneticthrombophilia should cause placenta deficienciesand intrauterine growth restriction by causing dis-orders during placenta thrombosis or placenta for-mation.11,12,14-16 But, in almost every case-controlcohort and studies examining low birth weightsand genetic thrombophilia intrauterine growthrestrictions are defined as the cases below the def-inite percentile fetal weight or standard deviation,cases detected placenta deficiencies are not sepa-rately defined. In actuality, most part of the infantsbeing smaller than expected according to the preg-nancy week, normal or abnormal, consists ofinfants structurally small.

Consequences of few studies classifying thecases by naming Doppler in English literature areinconsistent.5,8 In our study, thrombophilia inci-dence is stated for some group of low birthweighted infants having diastole end current lossof umbilical artery or inverse current.

MethodsResults relating to 17 patients that the genetic

thrombophilia tests were studied and cured fordiastole end current loss of umbilical artery orinverse current between the years 2003-2005 areretrospectively evaluated. Examined factorsinclude C resistance, protein C, protein S tests. Inaddition, lupus anticoagulant and anticardiolipin IgG, Ig M and anti phospholipids Ig G, Ig M testresults were also investigated.

Laboratory Method: Free protein S antigen wasmeasured by colorimetric method using enzymeelinked immunosorbent assay (ELISA)(Asserachrom free protein S, Diagnostica Stago,Asniéres, France) and Protein C Stachrom proteinC (Automated Coagulation Laboratory, DiagnosticaStago, Asnieres, France). APC resistance was mea-sured with STA®-Staclot® Protein C kit (PTT-LALupus Anticoagulant aPTT-based reagent,Diagnostica Stago, Asniéres, France). Plasma anti-cardiolipin and anti phospholipids antibody wasmeasured with commercial ELISA kits. Normal val-ues used for abnormal test results are given in theTable 1.

Study does not include a control group.Thrombophilia incidences informed in normalpopulation are used in order make a comparison.17-

19

ResultsList of the patients are given in the Table 2.

Weight of all the infants were under 5% accordingto their gestation weeks. None of the patients hadanti phospholipids antibody syndrome. In 11 of

Test Positive value

APC-R <120 sn

Pro C < %60

Pro S < %40

APTT-LA >48 sn

Anticardiolipin Ig G >12 MPLU/m

Anticardiolipin Ig m >12 GPLU/ml

Antiphospholipids Ig G >12 RU/ml

Antiphospholipids Ig m >12 RU/ml

Table 1. Reference values of the tests.


the patients at least one (64.7%), in three of themtwo genetic thrombophilia were seen (Table 3).When it is compared with the ratios declared forthe normal society, the ratio of thrombophilia wassignificantly higher for the patients in the workgroup (Table 3). The fourth, 6th, 7th and 8th casesthere were intrauterin exitus. Interestingly, three ofthese cases, thrombophilia were detected (6th, 7th

and 8th).

DiscussionIn our study, at least one thrombophic factor

was detected for the cases in a group whichintrauterine growth restriction was determined andhaving diastole end current loss in umbilical arteryor inverse current. FVL mutation studies of thepatients are not practiced, APC resistance resultsare available. While APC resistance is monitored inpregnancy especially for the older age pregnan-

cies, VL mutation is detected in most of the caseswhich APC resistance is determined. 7.1% carrierfrequency is declared for the FCL mutation of theTurkish society.21

In one of the early studies about the issue,Kupferminc et al detected at least one throm-bophilia as a ratio of 50% in 44 intrauterine growthrestriction cases.2 In this study, 66% of the infantswere born before 36th week and average infantweight was 1387 g Kupferminc et alcompared acase having placenta deficiency and seriousgrowth deficiency in the 22-26 pregnancy weekswith 52 normal pregnancies in their later publishedseries. Thrombophilia frequency was 69% for thegroup having growth deficiency and 14% for thecontrol group. 10 of the 13 infants recordedintrauterin exitus before the 25th pregnancy weekhad thrombophilia in accordance with our study.While 33% frequency of twice and more throm-bophilia factors were detected for the intrauterinegrowth restriction group, none of the patients inthe control group had thrombophilia.

Verspyck et al observed a relationship betweenintrauterine growth restriction and thrombophiliain a study including 203 infants having a fetalweight below 3%. Interestingly in this study, noneof the informed 34 infants having diastole end cur-rent loss had thrombophilia factors.8

Mc Cowan et al investigated the abnormalDoppler findings detected SGA infants separatelyin their study including 145 structurally smallintrauterine growth restriction cases and 290 nor-mal pregnant.9 When a general compare is donethought the study, there were no differencesbetween the infants SGA infants and control groupabout the thrombophilia incidence. But, theydeclared an increase in the frequency of throm-bophilia in a group of abnormal Doppler detectedinfants especially of the ones having a weight lessthan 3% although there was no statistically signifi-cant difference.

In a recent metaanalysis, the relationshipbetween FVL and prothrombin gene mutation andintrauterine growth restriction is searched.22 Whilea statistically significant heterogeneity between thestudies included in the metaanalysis was detected,it was stated that there should be a relationshipbetween prothrombin gene mutation and intrauter-

Nr APC-R Pro CR F-Pro S Pregnancy week Weight (g)

1 N N N 32 900

2 N N A 31 850

3 A N N 30 950

4 N N N 28 600

5 A N N 32 1100

6 A N A 27 400

7 A N A 31 900

8 N A N 32 720

9 N N N 31 1000

10 N A N 32 900

11 N N N 33 1200

12 N N A 34 1350

13 N N A 31 950

14 N N N 33 1200

15 A N A 33 1050

16 N N N 32 900

17 N N A 31 900

Tablo 2. List of the patients.

N: normal, A: abnormal

Test Case

n (%) Normal population (17-19)%

APC-R 5 (29.4) <15

Pro C 2 (11.8) 0.2-0.4

Pro S 7 (41.2) 0.3-0.13

Toplam 11 (64.7)

Table 3. Test results.

Atakan R et al., Frequency of Genetic Thrombophilia in Severe Intrauterine Growth Restriction140

ine growth restriction (OR approximately 2.4).Interestingly, when intrauterine growth restrictiondiagnosed series were separately evaluated for thefetal weights under 10 and 5%, relationshipbetween FVL/prothrombin gene mutation andintrauterine growth restriction existed only for theseries having the fetal weights under 5%. When itis considered that the cases of severe intrauterinegrowth restriction developed depending on theplacenta deficiency are most commonly seen forthe group having the fetal weights under 5%, it isseen that there should be a relationship betweensevere intrauterine growth restriction and FVL andprothrombin gene mutation.

In the present literature, there is no evidencesupporting the routine thrombophilia scanning forthe pregnancies which severe intrauterine growthrestriction is detected. We believe that the separateclassification of he cases which placenta deficien-cy is detected will help to clarify the subject.

References

1. Aktas F, Oral E. Kalitsal Trombofili ve Gebelik. Perinatolo-ji Dergisi 2002; 10: 4-10.

2. Kupferminc MJ, Eldor A, Steinman N, Many A, Bar-Am A,Jaffa A, et al. Increased frequency of genetic thrombophiliain women with complications of pregnancy. N Engl J Med1999; 340: 9-13.

3. Kupferminc MJ, Peri H, Zwang E, Yaron Y, Wolman I, El-dor A. High prevalence of the prothrombin gene mutationin women with intrauterine growth retardation, abruptioplacentae and second trimester loss. Acta Obstet GynecolScand 2000; 79: 963-7.

4. Martinelli P, Grandone E, Colaizzo D, Paladini D, Scianna-me N, Margaglione M, et al. Familial thrombophilia and theoccurrence of fetal growth restriction. Haematologica 2001;86: 428-31.

5. Kupferminc MJ, Many A, Bar-Am A, Lessing JB, Ascher-Landsberg J. Mid-trimester severe intrauterine growth rest-riction is associated with a high prevalence of thrombophi-lia. BJOG 2002; 109: 1373-6.

6. Nap AW, Hamulyak K, van Oerle R, van Pampus LC, Spa-anderman ME, Damoiseaux J, et al. Performance of a noveltest to quantify activated protein C resistance in womenwith a history of pre-eclampsia. Eur J Obstet Gynecol Rep-rod Biol 2004; 113: 26-30.

7. Rotmensch S, Liberati M, Mittlemann M, Ben-Rafael Z. Acti-vated protein C resistance and adverse pregnancy outcome.Am J Obstet Gynecol 1997; 177: 170-3.

8. Verspyck E, Borg JY, Le Cam-Duchez V, Goffinet F, DegreS, Fournet P, et al. Thrombophilia and fetal growth restric-tion. Eur J Obstet Gynecol Reprod Biol 2004; 113: 36-40.

9. McCowan LM, Craigie S, Taylor RS, Ward C, McLintock C,North RA. Inherited thrombophilias are not increased in"idiopathic" small-for-gestational-age pregnancies. Am JObstet Gynecol 2003; 188: 981-5.

10. Infante-Rivard C, Rivard GE, Yotov WV, Genin E, GuiguetM, Weinberg C, et al. Absence of association of thrombop-hilia polymorphisms with intrauterine growth restriction. NEngl J Med 2002; 347: 19-25.

11. Arias F, Romero R, Joist H, Kraus FT. Thrombophilia: amechanism of disease in women with adverse pregnancyoutcome and thrombotic lesions in the placenta. J MaternFetal Med 1998; 7: 277-86.

12. Salafia CM, Minior VK, Pezzullo JC, Popek EJ, RosenkrantzTS, Vintzileos AM. Intrauterine growth restriction in infantsof less than thirty-two weeks' gestation: associated placen-tal pathologic features. Am J Obstet Gynecol 1995; 173:1049-57.

13. Salafia CM, Pezzullo JC, Lopez-Zeno JA, Simmens S, MiniorVK, Vintzileos AM. Placental pathologic features of pretermpreeclampsia. Am J Obstet Gynecol 1995; 173: 1097-105.

14. Mousa HA, Alfirevic Z. Do placental lesions reflect throm-bophilia state in women with adverse pregnancy outcome?Hum Reprod 2000; 15: 1830-3.

15. Sikkema JM, Franx A, Bruinse HW, van der Wijk NG, deValk HW, Nikkels PG. Placental pathology in early onsetpre-eclampsia and intra-uterine growth restriction in wo-men with and without thrombophilia. Placenta 2002; 23:337-42.

16. Many A, Schreiber L, Rosner S, Lessing JB, Eldor A, Kupfer-minc MJ. Pathologic features of the placenta in women withsevere pregnancy complications and thrombophilia. ObstetGynecol 2001; 98: 1041-4.

17. Franco RF, Reitsma PH. Genetic risk factors of venousthrombosis. Hum Genet 2001; 109: 369-84.

18. Haverkate F, Samama M. Familial dysfibrinogenemia andthrombophilia. Report on a study of the SSC Subcommitteeon Fibrinogen. Thromb Haemost 1995; 73: 151-61.

19. Lindqvist PG, Svensson PJ, Marsaal K, Grennert L, LuterkortM, Dahlback B. Activated protein C resistance (FV:Q506)and pregnancy. Thromb Haemost 1999; 81: 532-7.

20. Bertina RM, Koeleman BP, Koster T, Rosendaal FR, DirvenRJ, de Ronde H, et al. Mutation in blood coagulation factorV associated with resistance to activated protein C. Nature1994; 369: 64-7.

21. Gurgey A, Mesci L. The prevalence of factor V Leiden (1691G-->A) mutation in Turkey. Turk J Pediatr 1997; 39: 313-5.

22. Howley HE, Walker M, Rodger MA. A systematic review ofthe association between factor V Leiden or prothrombingene variant and intrauterine growth restriction. Am J Obs-tet Gynecol 2005; 192: 694-708.



Abstract

Objective: The purpose of this study was to determine the serum levels of nitric oxide (NO) metabolites in pregnant womenwith preeclampsia and to find out any relation between the pathogenesis of preeclampsia and NO levels.

Methods: In this prospective, case-control study, venous blood samples were collected from pregnant women with preeclamp-sia (n=30) and age-matched healthy pregnant women (n=30). The serum fractions of these samples were assayed for total nit-rite/nitrate levels. The outcomes of the pregnancies were evaluated and groups were compared to each other for the clinicalcharacteristics and NO metabolites. Student’s paired t-test and χ2 test were used for the statistical analysis. P value less than0.05 was considered statistically significant.

Results: The mean total serum levels of nitrite/nitrate in pregnant women with preeclampsia and healthy pregnant women we-re 59.0 ± 15.55 µmol/L and 41.0 ± 10.37 µmol/L respectively. There were significantly higher total nitrite/nitrate levels in thematernal serum of preeclamptic women (p<0.05). Also, significantly higher nitrite/nitrate levels were found in severe preeclamp-tic women compared with those of mild preeclamptic and healthy pregnant women (p<0.05).

Conclusion: Maternal serum levels of NO metabolites were higher in pregnant women with preeclampsia and it was directlyrelated with the severity of the disease. This may be a compensatory mechanism to increase the blood flow to uteroplacentalunit in preeclampsia.

Keywords: Pregnancy, nitric oxide, preeclampsia, nitrite, nitrate.

Preeklampsili gebelerde maternal serum nitrik oksit metabolitlerinin seviyeleri

Amaç: Bu çal›flman›n amac›, preeklamptik gebelerdeki nitrik oksit (NO) metabolitlerinin serum seviyelerini tespit etmek ve NO se-viyesi ile preeklampsi aras›nda bir iliflki olup olmad›¤›n› ortaya ç›kartmakt›r.

Yöntem: Bu prospektif, vaka kontrollü çal›flmada preeklampsi tan›s› konulmufl gebe kad›nlardan (n=30) ve benzer yafl grubun-daki sa¤l›kl› gebelerden venöz kan örnekleri al›nd›. Al›nan kan örneklerinin serum fraksiyonlar›nda toplam nitrit/nitrat konsant-rasyonu hesapland›. Daha sonra her iki grupdaki gebeliklerin sonuçlar› araflt›r›ld› ve iki grup klinik özellikleri ile NO metabolitleriaç›s›ndan birbirleri ile karfl›laflt›r›ld›. ‹statistiksel de¤erlendirme için eflli t-test ve χ2 test kullan›ld›. 0.05’den küçük p de¤eri istatis-tiksel olarak anlaml› kabul edildi.

Bulgular: Preeklamptik ve sa¤l›kl› gebelerde ortalama toplam nitrit/nitrat seviyeleri s›ras›yla 59.0 ± 15.55 µmol/L ve 41.0 ± 10.37µmol/L olarak bulundu. Preeklamptik gebelerin maternal serumlar›nda toplam nitrit/nitrat seviyeleri anlaml› derecede daha yük-sekti (p<0.05). Ayr›ca fliddetli preeklampsi tan›s› alan gebelerdeki nitrit/nitrat seviyeleri, hafif preeklamptik ve sa¤l›kl› gebelerlekarfl›laflt›r›ld›¤›nda, anlaml› derecede yüksek saptand› (p<0.05).

Sonuç: Bu çal›flmada NO metabolitlerinin maternal serum seviyeleri preeklamptik gebelerde daha yüksek saptand› ve bu yüksek-lik preeklampsinin fliddeti ile do¤ru orant›l› olarak bulundu. Bu art›fl, preeklampside uteroplasental kan ak›m›n› art›rmaya yönelikkompensatuar bir mekanizma olabilir.

Anahtar Sözcükler: Gebelik, nitrik oksit, preeklampsi, nitrit, nitrat.

Maternal Serum Concentrations of Metabolitesof Nitric Oxide in Preeclampsia

Levent Tütüncü1, Emine Özdemir2, Ercüment Müngen1, Ali Rüfltü Ergür1, Yusuf Z. Yergök1

1Clinics of Gynecology and Obstetrics, GATA Haydarpafla Training Hospital, Istanbul2Clinics of Gynecology and Obstetrics, Gölcük Marin Hospital, ‹zmit

Correspondence: Dr. Levent Tütüncü, GATA Haydarpafla E¤itim Hastanesi, Kad›n Hastal›klar› ve Do¤um Klini¤i, ‹stanbul e-mail: [email protected]


IntroductionPreeclampsia is one of the most common he-

alth problems experienced by pregnant womenand it appears in approximately 5-8% of pregnan-cies later than 20 weeks.1 This disease which ischaracterized by hypertension, edema and prote-inuria is a very important pregnancy complicationwhich leads to both fetal and maternal morbidityand mortality by affecting all systems in the body.Even though etiology and pathogenesis of preec-lampsia could not been clarified definitely untilnow, it is considered that the basic problem is dec-reased placental bleeding appeared due to abnor-mal cytotrophoblast invasion and extensive endot-helium damage appeared dependent on this.2 Whi-le sensitivity of blood walls to angiotensin II withproduction of substances like this "endothelin" and"thromboxane" as a result of endothelium damage,it was indicated that production of vasodilatorsubstances like nitric oxide (NO) and prostacyclindecreased.3

NO which is synthesized from L-arginine,which is an amino acid, by the effect of “nitrite oxi-de synthase (NOS) enzyme is an effective free ra-dical which inhibits thrombocyte aggression andleads to vasodilatation in vessels.4 This very little li-pophilic molecule which was defined as “endothe-lium derived relaxing factor (EDRF)"5 in first yearsit was founded but then it was understood that thisis NO6,7 increases cyclic guanozine monophostate(cGMP) concentration by activating sithozolic gu-anilate cyclasis and thus leads to vasodilatation bydecreasing Ca++ level in-cells. NO is a gaseousmolecule, half-life of it is so short (nearly 4 se-conds) and rapidly converts into its metabolitesnitrite (NO2) and nitrate (NO3).8 For this reason, inmajority of studies in which NO production is re-searched concentration of its metabolites nitriteand nitrate was measured in different samples (ma-ternal plasma, serum, urine and various tissues,amniotic fluid, placenta, umbilical venous blood,cerebrospinal fluid).

It is known that both NO production and res-ponse to NO increase in normal pregnancy4,8 and itis though that this increase plays a role in manyphysiological mechanisms which provide continu-ation of the pregnancy.9 For this reason, there maybe a dysfunction appear in NO system in pathoge-nesis of preeclampsia and many studies have beenheld in this issue for recent 10 years.10 However,incompatible results were presented in these studi-

es held, and it is reported that NO level increasesin some pregnant women with preeclampsia,11,15

decreases in some of them,16,18 and does notchange in others.19,21

This study was planned with the aim of exhibit-ing whether or not changes in nitric oxide levelplay a role in pathogenesis of preeclampsia, and itdoes what is the relationship between severity ofpreeclampsia and nitric oxide levels, and totalserum nitrite nitrate levels were researched incases included in the study for this purpose.

Methods 30 pregnant women among those who applied

high-risk pregnancy polyclinic of our hospital anddiagnosed as preeclampsia and 30 pregnant wo-men as control group among those who appliedantenatal polyclinic and any problem was not bedetermined and who have similar characteristicswith study group were included in this study.Control group was formed among primigravidpregnant women who have applied our polyclinicby matching with pregnant women with preec-lampsia in terms of age, pregnancy week and riskfactors. The study was planned in accordance withprinciples of Helsinki declaration and permit docu-ment for study was obtained from ethic committeeof our hospital and “informed approval” documentwas taken from people who participated into thestudy. All pregnant women included in the studycomposed of primigravid women who have comp-leted 28th week of their pregnancy but have nothad a pregnancy later than 36th week, between 20and 35 ages, do not have therapy pregnancy, smo-king habit or another diagnosed systemic disease,risk factors like (diabetes mellitus, chronic hyper-tension, auto-immune diseases, chronic kidney fa-ilures, urinary infection, cardiovascular diseases,thyroid dysfunction, infective diseases etc.), do nottake any medical treatment other than iron and fo-lic acid, for whom any fetal anomaly was not diag-nosed and have monomer pregnancy.

ACOG criteria were used for preeclampsia di-agnosis.1 Accordingly tension arterial value, measu-red in sitting position at least for two times after a15 minute rest and in 6 hour intervals even thoughnormotensive is known before 20th week of preg-nancy, being higher than systolic 140 mmHg anddiastolic 90 mmHg and determining proteinuriahigher than 300mg in 24 hour urine was consid-ered as preeclampsia. In case tension arterial value

Tütüncü L et al., Maternal Serum Concentrations of Metabolites of Nitric Oxide in Preeclampsia144

measured in the same conditions is systolic 160mmHg, diastolic 110 mmHg, more than 5 g pro-teinuria is determined in 24-hour urine, urine out-flow lesser than 500 ml in 24 hour, fetal growingretardation, thrill or kidney dysfunction is deter-mined “severe preeclampsia” was diagnosed.

For all pregnant women included in study andcontrol groups full blood, full urine, kidney functi-on tests, liver function tests, preprandial blood su-gar, viral hepatitis indicators, indirect Coombs test,protein in 24-hour urine, creatine, urine cultureexaminations and fundus examination were held.In addition fetal monitor, ultrasonography and fe-tal Doppler researches were held in all of pregnantwomen in order to determine the situation of fetalwell-being. A diet lack of nitrite and nitrate (whichdoes not include spinach, beet and cooked meat)was given to all pregnant women included in thestudy for 24 hour and peripheral venous bloodwas drawn following an 8-hour hunger for the pur-pose of determining serum total nitrite/nitrate va-lue before starting any treatment for preeclampsia.Serum fractions of drawn blood were separatedand preserved at 70°C in order to research on massafter the end of study period.

Measurement of serum total nitrite/nitrate levelswas performed by a technician who is not infor-med about the study after all pregnant women hadprocreated. The method described by Cortas andWakid was used in measurement of serum totalnitrite/nitrate levels.22 This method is based onprinciple of degradation of nitrate to nitrite thro-ugh copper covered cadmium granules and me-asurement of obtained nitrite together with exis-ting nitrite in the atmosphere. The method of stan-dard adding was used in order to remove effect ofinhibitors like ascorbat etc.

All data in the study were given as ± standarddeviation. Statistical evaluations were conductedby using SPSS Ver. 11.0 (Chicago, IL, ABD) prog-ram, and independent groups with t-test ki squaretest, p<0.05 was considered statistically meaning-ful.

Results 30 pregnant women with preeclampsia 10

among which was diagnosed as slight, 20 as seve-re preeclampsia and 30 healthy pregnant womenas control groups were included in the study.When general characteristics of pregnant women

included in the study were decided, a significantdifference cannot be determined between preg-nant group with preeclampsia and healthy preg-nant women included in control group in terms ofpregnancy week in which samples were taken forcontrol of age and nitrite/nitrate serum levels(p>0.05). Nonetheless, average systolic and diasto-lic tension arterial values and protein amount de-termined in 24-hour urine were founded signifi-cant high in pregnant women with preeclampsiawho form study group (p<0.05). Pregnancy periodin pregnant women with preeclampsia and avera-ge birth weight of newborn babies were also foun-ded significant lower compare to control group(p<0.05). In addition, 63.3% caesarean rates instudy group was determined significant highercompare to control group in which this rate is33.3% (p<0.05). While perinatal in one pregnantand postnatal fetal loss in one pregnant was obser-ved in the study group, no fetal loss was observedin pregnant women included in control group.General characteristics of pregnant women inclu-ded in the study and differences between the gro-ups were presented in Table 1.

Maternal serum average nitrite/nitrate level inpregnant women with preeclampsia who formstudy group was founded as 59.0 ± 15.55 µmol/L.this values was determined as 41.0 ± 10.37 µmol/Lin the control group and there was a statisticallysignificant difference between two groups (p<0.05)(Table 2). When mild and severe preeclampticpregnant women were evaluated separately mater-nal serum average nitrite/nitrate values were deter-mined respectively as 51.8±13.63 µmol/L and73.8±6.0 µmol/L. The value determined in the gro-up with severe preeclampsia was a significant hig-her value statistically compare to both the groupwith mild preeclampsia and the control group(p<0.05).

Discussion In many studies conducted until now it was

declared that NO production increases at least invessel bed and uterus during pregnancy periodand this increase ensures uterus to keep silent bydecreasing contractility until accouchement activi-ty starts and plays an important role in adaptationof vascular structures in pregnancy.4,8 In researchesconducted for this purpose, it was indicated thatcGMP and nitrite/nitrate amount in plasma andurine in normal pregnancies and thus NO produc-

tion also increases.9 Setting out from this point theidea that there may be a decrease in NO producti-on in explanation of clinic findings appeared inpregnant women with preeclampsia unlike normalpregnant women was come up and for this purpo-se tens of studies were conducted and publishedoriented to exhibit possible role of NO system inpreeclampsia.10-21 In majority of these studies NO2

and/or NO3 levels were searched rather than NOhalf-life of which is so short in maternal and fetalplasma.11-14,16-21 In addition to this, some studies ha-ve been published in which NO metabolites in am-nious fluid,23 brain-spinal cord fluid24 or cord blo-od12,15 of pregnant women with preeclampsia weresearched. As a result of these studies incompatibleresults were reported and even though it was ex-hibited that NO system may play a role in patho-genesis of preeclampsia, it was not clarified howthis occurs. For this purpose in studies recentlyheld with higher-techniques NOS isoenzymeswhich take a role in NO synthesis were researchedrather than NO metabolites, but again different re-sults have been reported and it was declared that

NOS mRNA production decreases25 or does notchange in pregnant women with preeclampsia26 orthere is no difference in NOS isoenzyme levelswhich is examined with immune dying betweenpreeclamptic and normotensive pregnant women.27

In our study on the other hand, maternal serumaverage nitrite/nitrate levels in preeclamptic preg-nant women were found meaningfully high com-pare to normotensive healthy pregnant women.When the effects of NO is taken into considerationit is expected that decrease in NO efficiency in apreeclamptic pregnant and vasoconstriction appe-ar dependent on this should play a role in patho-genesis of preeclampsia, on the contrary increasein NO metabolites makes us to think that NO sys-tem does not have a direct role on pathogenesis ofpreeclampsia, rather this is a compensator mecha-nism oriented to decrease emerged preeclampsiafindings and increase utero-placental blood stre-am. This result also complies with some studiesheld before.11-14 In addition higher NO metabolitelevels found in severe preeclampsia group in our


Characteristic Preeclampsia Normal pregnancy P value

(n=30) (n=30)

Age (year) (Average±SD) 29.06±5.40 28.06±4.01 ad

Pregnancy week when the sample is taken(Average±SD) 32.6±2.8 32.1±3.0 ad

Pregnancy week in accouchement (Average±SD) 35.2±2.7 38.1±2.1 <0.05

Systolic blood pressure (mmHg) (Average±SD) 153±19 114±8 <0.05

Diastolic blood pressure (mmHg) (Average±SD) 113±14 73±6 <0.05

Protein in 24-hour urine (g) (Average±SD) 4.28±1.02 0.18±0.22 <0.05

Birth weight (g) (Average±SD) 2488±751 3226±276 <0.05

Cesarian accouchement rate 19 (%63.3) 10 (%33.3) <0.05

Perinetal death 2 (%6.66) 0 ns

SD: Standard deviationns: Not significant

Table 1. General characteristics of pregnant women included in the study.

Maternal serum average

nitrite/nitrate amount (µmol/L)

Preeclampsia (n=30) 59.0±15.55a

Mild preeclampsia (n=10) 51.8±13.63a

Severe preeclampsia (n=20) 73.8±6.0a,b

Normal pregnancy (n=30) 41.0±10.37

P value <0.05

Note: Values are presented as average±standard deviation. a: Significant compare to control group (p<0.05)b: Significant compare to mild preeclamptic group (p<0.05)

Table 2. Maternal serum nitrite/nitrate concentrations.

study can be considered as a finding which sup-ports this thought. Similarly, Pathak et al havefounded serum nitrite/nitrate levels in preeclamp-tic pregnant women significant higher compare tonormotensive pregnant women in their study anddeclared that they determined direct proportionbetween the severity of preeclampsia and nitri-te/nitrate levels.28 Shaamash et al have also indica-ted in their study held in 2000 there is a positivecorrelation between the severity of preeclampsiaand the amount in maternal fetal circulation of NOmetabolites.12 Even in a study, which declared thatany difference was not detected between preec-lamptic pregnant women and normotensive onesin terms of serum nitrite/nitrate levels, NO produc-tion was found higher in severe preeclampsia gro-up.21 All these findings are findings which supportthe result determined in our population and whichindicates that the higher the severity of preeclamp-sia the higher NO production occurs.

It has been maintained that this increase in NOproduction and oscillation occur depending on en-dothelium damage and oxidative stress appear inpreeclamptic pregnant women, and it was alsothought that thrombocytes, trophoblasts, desidualand myometrial cells may also be reasons of incre-ased NO production.13 Excess NO secreted fromthese sources may be a compensator mechanismoriented to increase vasoconstriction, thrombocyteaggression appear in pregnant women and utero-placental blood stream decreased as a result ofthis. It was contended that pregnant women withpreeclampsia pass through four different periodstheoretically and according to this hypothesis itwas affirmed that the period in which any findinghas not been detected before estimated factoremerged constitutes the first phase, the period inwhich any clinic finding has not emerged since thebalance was continued with compensator mecha-nisms after the estimated factor emerged constitu-tes the second phase, the period in which severefindings have not been determined since compen-sator mechanisms were still effective even thoughmild clinic findings emerged constitutes the thirdphase, and the period in which compensator mec-hanisms were not sufficient any more and severeclinic findings have been determined constitutesthe fourth phase.8 According to hypothesis bases ofcompensator mechanisms in the second and thirdphases are formed by NO system, after possible

factor which leads to preeclampsia emerges NOproduction and oscillation starts to increase and itprevents severe findings to emerge until last pha-ses of pregnancy, however this cannot be suffici-ent after a certain stage even though NO levels areso high and then picture of severe preeclampsiaemerges. The findings obtained in our study alsosupport this hypothesis.

Conclusion In this study total nitrite/nitrate levels in mater-

nal serums of preeclamptic pregnant women werefound meaningfully high compare to normotensivehealthy pregnant women. This high level increasein direct proportion with severity of preeclampsia.In preeclampsia which is one of the most seriousproblems appear in pregnant women NO systemmay play a preventive role directed to increaseutero-placental blood stream. However, studieswhich can directly indicate NO levels in differentperiods of pregnancy are required in order to de-termine the definite role of NO in preeclampsiapathogenesis.

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Abstract

Objective: To investigate the results of therapeutic modalities in second trimester twins, following the birth of the first twin.

Methods: Seven cases were investigated for their clinical features and prognosis, in which cases either active conservative treat-ment was implemented following the birth of first twin or no treatment was implemented to delay the birth of second twin.

Results : The mean gestational week was 18.7 ± 4.1 (13-26). All four cases of no treatment were miscarried. The deliveries ofthe other three pregnancies with emergency cerclage, were delayed by 2, 40 and 42 days. In these cases, the perinatal prog-nosis was unsuccessful; however there were no maternal complicatioins.

Conclusion: For multiple pregnancies with limited survivability, delayed delivery of the second twin could be tried; the resultof prognosis may not be positive in all cases.

Keywords: Multipl pregnancy, selective delivery, emergency cerclage, delayed delivery of second twin, conservative manage-ment.

Gebeli¤in ikinci trimesterinde ikizlerden birinin do¤umunu takiben konservatif yaklafl›m

Amaç: ‹kinci trimester ikizlerde birinci fetüsün do¤umunu takiben tercih edilen tedavi seçeneklerinin sonuçlar›n›n araflt›r›lmas›.

Yöntem: Birinci fetüsün do¤umundan sonra aktif konservatif tedavi yap›lan veya herhangi bir tedavi uygulanmayarak ikincifetüsün do¤umu geciktiren yedi vaka klinik özellikleri ve prognoz yönünden irdelendi.

Bulgular: Gebelik haftas› ortalama 18.7 ± 4.1 (13-26) bulundu. Konservatif davran›lan olgular›n dördü de kaybedildi. Acil serk-laj uygulanan üç gebelikte ikinci fetüsün do¤umu 2, 40 ve 42 gün süre ile geciktirilebildi. Bu olgularda perinatal prognoz olum-suz olmakla birlikte maternal komplikasyona rastlanmad›.

Sonuç: Yaflayabilirlik s›n›r›na yak›n ikizlerde ikinci fetüsün geciktirilmifl do¤umu denenebilir, ancak prognoz her zaman yüzgüldürücü olmayabilir.

Anahtar Sözcükler: Ço¤ul gebelik, selektif do¤um, acil serklaj, ikizlerde geciktirilmifl do¤um, konservatif yaklafl›m.

Conservative Managemenet of Twin PregnancyAfter Delivery of One Fetus at the Second

Trimester of the Pregnancy


Clinics of Gynecology and Obstetrics, Haseki Training and Research Hospital, ‹stanbul

Correspondence: Dr. Cem Dane, Haseki E¤itim ve Araflt›rma Hastanesi, Kad›n Hastal›klar› ve Do¤um Klini¤i, ‹stanbule-mail: [email protected]

IntroductionThe frequency of multi-fetal pregnancies have

increased significantly in the last 20 years becauseof ovulation induction and IVF.1 multi-fetal preg-

nancies carry high risk of premature birth and as a

result of perinatal morbidity and mortality.2 In

these pregnancies following the delivery of the

first fetus the other fetus or fetuses are born a short

time after. Usually because of premature birth theprolongation of the time between the delivery ofthe fetuses and viability of the fetuses born after israre.3 there is no consensus on the procedures thatcan be performed following the birth of one of thetwins to prolong the gestation for the unborn fetus.For this purpose interventions like emergency cer-clage, tocolysis have been tried and 2 to 107 dayswere gained and the prognosis of the newbornsvaried.4,5

In this presentation, we aimed to investigatethe effects of the approaches taken in diamniotic-dichorionic cases where only one fetus were bornto the duration and prognosis of the pregnancies.

MethodsBetween the years 2000 and 2004, in seven

twin pregnancy cases attending with a threat ofabortion or premature birth in the first or secondtrimester of pregnancy, with the first fetus deliv-ered and the second followed up in our clinic,demographic data, the clinical approaches thatwere followed, methods of intervention, the lengthof time the pregnancies could be prolonged andthe morbidity and mortality of the pregnantwomen and fetus were assessed retrospectively.Cases in which active conservative approach wastaken and spontaneous follow up was done wereselected randomly.

ResultsIn the cases investigated the gestational week

was between 13 and 26, in average was 18.7 ± 4.1.The average age of the women were 27.8 ± 5.9(18-34). The average number of pregnancies was2.8 ± 1.8, the number of children living were 1.4 ±1.5. Two patients were nullipara; the other 5 pati-ents were multipara. Two of the women achievedpregnancies after infertility treatment (Table 1).

In all of the cases except one both of the fetu-ses were alive and all the pregnancies were dicho-rionic diamniotic. While four of the cases were fol-lowed up spontaneously cerclage was performedin three. The families requested that the pregnancybe prolonged, cerclage was recommended by us,but important risks such as sepsis were explainedin detail and consent was taken before the proce-dure. In the three cases in which emergency cerc-lage were preformed all the procedure was perfor-med under general anesthesia in operation roomsand smear was taken for bacteriological investiga-tions in trandelenburg position. Following the liga-tion of the umbilical cord from above with a mate-rial that is not absorbed, front and back cervixwalls were caught by forceps, 5 mm Mersilene Ta-pe (Ethicon RS-21, Ethicon Inc, Somerville, NewJersey, USA) was used and ligation was done withthe Mc Donald method. Indometacin and nifedip-ine were given to the patients who had cerclagebefore the 20th gestational week as tocolytics andafter the 20th week parenteral ritodrin was given.

Age Case G,P,C Gestational Cerclage Tocolysis Antibiotic Birth Apgar Delay Survival

age weight (g) score (1’-5’) (day)

1 25 4,3,0 17 Mc Donald Nifedipine Ampicillin

Indometacin Metranidazole 150 / 550 4/2 42 - / -

2 32 2,0,1 13 Mc Donald Nifedipine Ampicillin

‹ndometacin Metranidazole 80/280 0/0 40 -/-

3 23 1 20 Mc Donald Ritodrin Ampicillin

Metranidazole 320/380 4/0 2 -/-

4 34 4,3 21 Not done Not done Ampicillin


5 31 6,3,2 26 Not done Not done Ampicillin


6 32 2,1 18 Not done Not done Ampicillin


7 18 1 16 Not done Not done Ampicillin


Table 1. Following the birth of one of the twins demographic characteristics cases that cerclage is performed and not performed.


Prophylactic antibiotic (ampicillin + metronida-zole) for 10 days was planned for all the patientsand even if there was an abortion this treatmentwas used. In daily follow up the fetal heart soundsfever, uterine sensitivity, control of discharge andleucocyte number were examined. All the patientswere hospitalized following the birth of the first fe-tus. Usually going back to everyday activities werepermitted within a week as vaginal discharge dec-reased. The women who left the hospital after 10days were followed by weekly ultrasonography forfetal parameters, for infection criteria tests wereperformed first weekly than once in 15 days.

The four cases followed up conservatively hadabortion or delivery within 3 to 7 days. In two ofthe three cases in the cerclage group a duration of40 and 42 days were gained, one case had aborti-on within 48 hours. All the fetuses were born withvaginal labor. The first minute and fifth minute Ap-gar scores of all the fetuses were under 5. Of thefirst fetuses born four were born vaginally, fourmales and three females. Among these one wasdead at birth; others were alive but were lost wit-hin the first 24 hours. In all the cases the reason ofdeath was high degree of prematurity. The intervalbetween the first fetuses and the ones born afterbeing delayed was between 2 and 42 days (28.0 ±22.5). In the postpartum assessment of the placen-tas all were found to be diachronic. Significant ma-ternal morbidity was not seen in those who hadserclage and those who did not have during thefollow up time and post abortion-birth.

DiscussionIn multi-fetal pregnancies the expectation as a

result of premature rupture of membranes in thesecond trimester is the delivery of the fetuses withshort intervals. Sometimes following the birth ofthe first fetus contractions may cease. The com-mon approach today is to facilitate the birth of thesecond fetus because of poor results.6 In 1880 Car-son 1880 published the first case where 44 dayswere present between the birth of the twins.7 In1994 Kalchbrenner et al developed a protocol fordelaying birth and the cases to be selected.8 Accor-ding to this:

1. The multi-fetal pregnancy should be betwe-en 18 and 24 weeks,

2. The second pregnancy should be diamniotic,

3. The pregnancy sac to be preserved shouldnot be damaged,

4. These should not exist: fetal distress, placen-

ta decolmant and intraamniotic infection. Althoughin literature presentations made on this subject andmany retrospective case series are present there isno randomized trial conducted. Especially there isno controlled study comparing emergency cercla-ge with prophylactic cerclage or bed rest.9 becauseof this in terms of proof dependent medicine ma-king the last decision in solving this problem doesnot seem possible. Novy compared 39 second tri-mester cases with emergency cerclage with 31 se-cond trimester cases who had bed rest, in the gro-up who had cerclage fetal survival was 80% and inthe other group 75%.10 In another study fetal survi-val in 20 emergency cases were found to be 55%,11

and in 32 second trimester emergency cerclage ca-ses 48% fetal survival was detected.12 the averageprolongation times of the above pregnancies werestated as 1 to 14 days. These comparisons do notgive net results to the clinicians for the manage-ment of such conditions because the case groupsare small, selection criteria are in sufficient andthere is prejudice in selection.

In our cases especially in the smallest one thefact that the pregnancy was achieved after IVF andthe persistent behavior of the family caused cerc-lage to be performed at the very beginning of thesecond trimester, the pregnancy could be prolon-ged until the 20th week, but could not be prolon-ged longer. Under intensive follow up conditionsand close clinical follow up a 2 to 42 day delay inthe pregnancies we followed up was possible.This interval was longer in those who had a cerc-lage. In the pregnant women we investigated nocomment on survival could be made because thedelivery times were very early.

There are not enough data to decide on the ad-vantage of prophylactic antibiotic use in emer-gency cerclage cases. Of the three studies conduc-ted on this subject two are for the use of prophy-lactic antibiotics and one is against.13-15 we prefer-red using prophylactic antibiotics.

In literature there is also no consensus on theusage of prophylactic tocolytic therapy to delaythe birth of the second twin. In a study conductedprophylactic tocolysis had positive input to the 23of the 25 patients.16 In his own series Wittmannthinks that tocolysis is not helpfull.17 we used indo-metacin, nifedipine and after the 20th week paren-teral tocolysis in our cases and were successful intwo of the three cases in short and middle term.

Some researches let the patients exit the hospi-tal after the cerclage. We preferred 10 days of hos-

Dane C et al., Conservative Managemenet of Twin Pregnancy After Delivery of One Fetus at the Second Trimester150

pitalization and bed rest, and performed weeklyfollow ups in the next period.

Under the conditions of our country emergencycerclage should not be accepted as a standard app-roach to prolong the intervals between deliveriesin pregnancies less than 24 weeks. But after the24th week when fetal viability starts it could be amethod that improves the prognosis of the fetus bypreventing the complications of premature birth.In our cases emergency cerclage did not preventpremature birth but prolonged the duration of thepregnancy. Although the number of cases werelow, this prolonged time seems to improve the sta-tus and life conditions of the infant born prematu-rely because the application date is in more advan-ced gestational weeks. Besides, this additional timegained may provide time for the corticosteroidsused to mature the fetal lungs. In such situationsthe risk of the premature birth of the baby and therisk of the anesthesia and tocolysis applied to themother must be balanced. Risks should be expla-ined and the patient should be prepared psycholo-gically.

ConclusionDelayed premature labor may be a beneficial

approach in twin pregnancies in which one of thefetuses are born. This management strategy is ge-nerally referred to as conservative therapy. Activeconservative therapy, bed rest, continuous hospita-lization or hospitalization in intervals, high ligationof the umbilical cord of the first twin born, tokoly-tic therapy, antibiotic therapy either continuous orat intervals, in addition starting corticosteroids af-ter 26th week, although there is no net consensuscerclage may be preferred in these cases. Regularclinic and ultrasonographic examinations and la-boratory follow up should be done for the signs ofchorioamnionitis that is a contraindication for con-servative therapy. Because such pregnancies arenot encountered frequently prospective studies aredifficult to make and only retrospective studies canbe found on this subject. In the studies publishedthere is not enough information about the mediumand long term development of the surviving ne-onates. Although restricted the information obta-ined from these small series show that pregnanci-es can be extended in the second trimester until40-42nd day. After the 22-24th gestational weekssuch interventions conducted at tertiary centersmay be helpful in some cases with the as long asinformed consent is taken. But it must be remem-

bered that interventions performed previously maycause harm instead of help.

References

1. Callahan TL, Hall JE, Ettner SL, Christiansen CL, GreeneMF, Crowley WF Jr. The economic impact of multiple-ges-tation pregnancies and the contribution of assisted-repro-duction techniques to their incidence. N Engl J Med 1994;331: 244-9.

2. Mercer BM, Crocker LG, Pierce F, Sibai BM. Clinical charac-teristics and outcome of twin gestation complicated by pre-term premature rupture of the membranes. Am J ObstetGynecol 1993; 168: 1467-73.

3. Rutter N. The extremely preterm infant. Br J Obstet Gyna-ecol 1995; 102: 682-7.

4. Zhang J, Hamilton B, Martin J, Trumble A. Delayed intervaldelivery and infant survival: a population-based study. AmJ Obstet Gynecol 2004; 191: 470-6.

5. Oyelese Y, Ananth CV, Smulian JC, Vintzileos AM. Delayedinterval delivery in twin pregnancies in the United States:Impact on perinatal mortality and morbidity. Am J ObstetGynecol 2005; 192: 439-44.

6. Clerici G, Cutuli A, Renzo GC. Delayed interval delivery ofa second twin. Eur J Obstet Gynecol Reprod Biol 2001; 96:121-2.

7. Carson JCL. Twins born with an interval of forty-four days.BMJ 1880; 1: 241-2.

8. Kalchbrenner MA, Weisenborn EJ, Chyu JK, Kaufman HK,Losure TA, Losure TA. Delayed delivery of multiple ges-tation: maternal and neonatal outcomes. Am J ObstetGynecol 1998; 179: 1145-9.

9. Drakeley AJ, Roberts D, Alfirevic Z. Cervical stitch (cerc-lage) for preventing pregnancy loss in women. CochraneDatabase Syst Rev 2003; (1): CD003253.

10. Novy MJ, Gupta A, Wothe DD, Gupta S, Kennedy KA,Gravett MG. Cervical cerclage in the second trimester ofpregnancy: a historical cohort study. Am J Obstet Gynecol2001; 184: 1447-54.

11 Lata RA, McKenna B. Emergent cervical cerclage: predictorsof success or failure. J Matern Fetal Med 1996; 5: 22-7.

12. Lipitz S, Libshitz A, Oelsner G, Kokia E, Goldenberg M,Mashiack S, et al. Outcome of second-trimester emergencycervical cerclage in patients with no history of cervical in-competence. Am J Perinatol 1996; 13: 419-22.

13. Long MG, Gibb DM, Kempley S, Cardozo LD, Nicolaides K,Gamsu H. Retention of the second twin: a viable option?Case report. Br J Obstet Gynecol 1991; 98: 1295-9.

14. Antsaklis A, Daskalakis G, Papageorgiou I, Aravantinos D.Conservative treatment after miscarriage of one fetus inmultifetal pregnancies. Fetal Diagn Ther 1996; 11: 366-72.

15. Bakos O, Cederholm M, Kieler H. Very prolonged memb-rane rupture and delayed delivery of the second twin. FetalDiagn Ther 1998; 13: 147-9.

16. Fayad S, Bongain A, Holhfeld P, Janky E, Durand-Reville M,Ejnes L. Delayed delivery of second twin: a multicentrestudy of 35 cases. Eur J Obstet Gynecol Reprod Biol 2003;109: 16-20.

17 Wittmann BK, Farquharson D, Wong GP, Baldwin V, Wads-worth LD, Elit L. Delayed delivery of second twin: report offour cases and review of the literature. Obstet Gynecol 1992;79: 260-3.



Abstract

Objective: To investigate the incidence of early diastolic notch in uterine artery Doppler measurements and analyze relation-

ship of early diastolic notch with perinatal outcome such as preeclampsia, preterm delivery, intrauterine growth retardation,

neonatal birth weight and apgar scores.

Methods: Two hundred sixty-one pregnant women underwent uterine artery Doppler measurements at 24 weeks of gesta-

tion. Patients were divided in two groups. Group 1: Early diastolic notch negative and group 2: Early diastolic notch positive.

The relationship between early diastolic notch and perinatal complications were assessed prospectively.

Results: Of 243 consecutive pregnancies, early diastolic notch was observed in 41 (16.8%) patient. Mean value of uterine artery

pulsality indices, resistivity indices and neonatal birth weight were statistically different between the two groups (p = 0.00).

Preeclampsia, and preterm delivery were significantly frequent in group 2.

Conclusion: Diastolic notch might be an important indicator for early identification adverse perinatal outcomes such as preterm

birth, intrauterine growth retardation.

Keywords: Doppler ultrasonography, diastolic notch, perinatal outcome.

Düflük riskli gebelerde arteria uterina’da elde edilen erken diyastolik çentiklenmenin gebeliksonuçlar› ile iliflkisi

Amaç: Doppler ultrasonografide arteria uterina’da elde edilen erken diyastolik çentiklenme s›kl›¤›n›n saptanmas› ve erken diyas-

tolik çentiklenme varl›¤›n›n, fetal do¤um a¤›rl›¤›, do¤um sonras› apgar skorlar›, erken do¤um, intrauterin geliflme gerili¤i ve pre-

eklampsi geliflimi gibi perinatal sonuçlar ile iliflkisinin araflt›r›lmas› amaçland›.

Yöntem: Antenatal poliklini¤ine baflvuran düflük riskli tek fetus gebeli¤i olan, 261 olguya 24. gebelik haftas›nda ultrasonogra-

fik inceleme yap›ld›. Anomali tespit edilmeyen gebelere bilateral uterin arter Doppler kan ak›m analizi yap›ld›. Prospektif olarak

olgular iki gruba ayr›ld›. Grup 1: Erken diyastolik çentiklenme izlenmeyen grup ve Grup 2: Erken diyastolik çentiklenme izlenen

grup. Daha sonra bu gebelikler do¤uma kadar takip edilerek perinatal sonuçlar belirlendi.

Bulgular: Doppler ultrasonografisi yap›lan 243 gebenin 41’inde (%16.8) Erken diyastolik çentiklenme izlendi. Grup 1 ve grup

2’de yenido¤an do¤um a¤›rl›klar› (p = 0.00), uterin arter Pulsatilite indeksi ve Rezistans indeksi de¤erleri aras›nda (p = 0.00) is-

tatiksel olarak anlaml› fark tespit edildi. Preeklampsi, düflük do¤um apgar skoru ve erken do¤um aç›s›ndan grup 1 ve grup 2 ara-

s›nda istatiksel olarak anlaml› fark saptand›.

Sonuç: Düflük riskli gebelerde geliflebilecek preeklampsi, intrauterin geliflme gerili¤i, erken do¤um gibi komplikasyonlar için an-

tenatal takip s›ras›nda Doppler ultrasonografide uterin arterde çentiklenme varl›¤› önemli bir bulgu olabilir.

Anahtar Sözcükler: Doppler ultrasonografi, diyastolik çentiklenme, perinatal sonuçlar.

Relationship of Early Diastolic Notch in UterineArtery Doppler Measurements With Pregnancy

Complications in Low Risk Pregnancies

Faik Gürkan Yaz›c›1, Ekrem Tok1, S›tk› Gülhan2, Devrim Ertunç1, Gülay Özdemir1, Saffet Dilek1

1Department of Gynecology and Obstetrics, Faculty of Medicine, Mersin University, Mersin2Department of Radiology, Faculty of Medicine, Mersin University, Mersin

Correspondence: Dr. Faik Gürkan Yaz›c›, Mersin Üniversitesi, Kad›n Do¤um Anabilim Dal›, Mersin, e-mail: [email protected]

IntroductionDiseases that may be causes of perinatal morta-

lity and morbidity such as preeclampsia, intrauteri-ne growth retardation (IUGR) are often seen in thethird month or even just before the time of birth.Pathophysiologic mechanisms are believed to ori-ginate at the earlier times in pregnancy.1,2 Duringthe period of a normal pregnancy beginning fromthe first three months till the 24th week, becomingmore evident as time goes by, there is an increasein the diastolic blood flow of the uterine vessels.The high resistant blood flow seen in the uterineartery untill 12-14 week pregnancy is replaced bythe low resistant flow after trophoblast invasion inthe spiral arteries takes place.3

In the patients who are determined to havehigh resistance index (RI) and high pulsatility in-dex (PI) in Doppler ultrasound examinations, thefrequency to have preeclampsia, IUGR and placen-tal failure compared to the ones who have normalDoppler ultrasound findings has been found to behigher.4 Early diastolic notch (EDN) within the ute-roplacental Doppler flow curves during the secondhalf of pregnancy shows a pathologic flow turn inthe spiral artery region, probably due to inadequ-ate trophoblast invasion during the time of placen-tal formation.

In this study the objective was to study,at the24th week, the incidence of early diastolic notch inuterine artery Doppler measurements and analyzerelationship

of early diastolic notch with perinatal outcomessuch as preeclampsia, preterm delivery, intrauter-ine growth retardation, neonatal birth weight andapgar scores of the low risk population of preg-nants who applied to the policlinic.

MethodsThe low risk pregnants, who applied to the an-

tenatal clinics of the Department of Gynaecologyin Mersin University, Faculty of Medicine betweenJuly 2003 and June 2004 got involved in this study.Doppler ultrasound examination was applied to261 patients, in whom no fetal anomaly had beenobserved by ultrasound examination, who did nothave preeclampsia, IUGR, preterm delivery, historyof intrauterine death, systemic diseases such as

chronic hypertension, diabetes and kidney diseaseand risk factors during their previous pregnancy,and who had one fetus, at the 24th week of preg-nancy. The results of pregnancy could not be reac-hed in 18 patients, because some did not apply toMersin University Hospital for their follow-ups,and some had the antenatal follow-ups at otherhospitals. The results of 243 cases, whose measu-rements were taken by Doppler ultrasonography atthe 24th week and whose perinatal results couldcompletely be obtainded, were studied. All of thepatients, who got involved in the study, were gi-ven approval forms, as demanded by Mersin Uni-versity ethics committee.

Technics: Ultrasonography and Doppler me-asurements werre applied to all of the patients bythe same person (GÖ). For the ultrasonographymeasurements General Electric Logic 500 Pro ultra-sound machine (Wi, USA) and C357 abdominalprobe were used. All of the pregnant women res-ted by sitting for about 15 minutes before Dopplerultrasonography examination took place, and blo-od pressure levels were taken. First fetal biometrymeasurements were made. Analysis of both uteri-ne artery blood flow were made for patients withpregnancy time corresponding to 24th gestationalweek and the ones who had no considerable cons-titutional anomaly. By using Color Doppler ultraso-nography, the place, where uterine arteries crossthe the external illiac arteries, was determined. Byusing “cut-flow” pulse-wave Doppler, flow ratewave forms at the portion of the artery on the si-de of uterus was recorded.5 RI and PI values ofright and left uterine arteries were evaluated sepa-rately. After consecutive five waves were obtained,according to presence of EDN, cases were dividedinto two groups. Group 1: Group without EDN andGroup 2: Group with EDN (Diagram 1). Then the-se pregnancies were followed untill birth.

For the determination of perinatal outcomes,hospital records and the information taken fromparents were used. The cases, who had systolicpressure > 140 mmHg and/or diastolic pressure>90 mmHg and ≥ 500 mg/day proteinuria, wereaccepted to have preeclampsia 6. Delivery before37th week was defined as preterm delivery andbirth weight under 10th percentile with respect toexpected gestational week was defined as IUGR.The limit to be accepted as low birth apgar scorewas 5th minute apgar score ≤ 7.


The frequency of unilateral and bilateral EDN atthe 24th week was calculated. Statistical analysiseswere made by using “Student’s t-test” and the pe-centage comparison was made by using ki-squaretest. In all groups uterine artery Doppler analysisresults and perinatal outcomes were compared.The effect of the presence of EDN on perinataloutcomes such as newborn apgar scores, birthweight and preterm delivery was studied.

ResultsIn 202 of 243 pregnant women (83.1%) diasto-

lik EDN was not observed (group 1). In 41 of 243pregnant women (16.8%) EDN was observed(group 2). EDN was seen 9.46% bilaterally and7.41% unilaterally. In the group, in which EDN wasnot seen, 75 women were primigravida (37.1%),127 women were multipar (62.8%) and the averageage was 27.7 ± 5.0. Average value of PI of uterineartery at ultrasound Doppler examination wasfound to be 0.87 ± 0.36 and the average value ofRI 0.52 ± 0.11. The average birth weight of thenewborns was 3106 ± 264 (Table 1). In group 2 25of the pregnant women (61 %) were multipar and16 (39 %) of them were primigravida, the averageof ages of the mothers was 26.9 ± 5.0. In thegroup, in which EDN was seen, the average of PIvalues was 1.45 ± 0.61 and the average of RI val-ues was 0.67 ± 0.13. The average of the weight ofthe newborns was 2945 ± 527. There was no con-

siderable statistical difference of patient ages bet-ween the groups with EDN and without EDN(p=0.32). There was considerable statistical dif-ference of newborn birth weights (p=0.00) and theaverage of PI and RI values of uterine arterybetween two groups.

When perinatal outcomes were evaluated in thegroup without EDN, preeclampsia rate was foundto be 3.4%, IUGR 3%, low apgar score 1.4 %,preterm delivery 8.4% and cesarean section 16%(table 2). In the group with EDN, preeclampsiarate was found to be 12.9%, IUGR 9.8%, low apgarscore 7.3%, preterm delivery 21 % and sectio 24%(Table 2). There was no considerable statistical dif-ference of cesarean section rates between thegroups with EDN and without EDN (p=0.15).There was significant statistical difference of lowapgar score at birth and preterm delivery betweentwo groups (Table 2).

Figure 1. Early diastolic notch at the uterine artery Doppler ultrasound.

Group 1 Group 2 P value

(n=202) (n= 41)

Average of age (year) 27.7 ± 5.0 26.9 ± 5.0 0.32

Pulsatility index 0.87 ± 0.36 1.45 ± 0.61 0.00

Resistance index 0.52 ± 0.11 0,67 ± 0.13 0.00

Birt weight (gramm) 3106 ± 264 2945 ± 527 0.00

Table 1. Comparison of averages of PI, RI and newbornbirth weight in Groups 1 and 2 (average ± standarddeviation).

Yaz›c› FG et al., Relationship of Early Diastolic Notch in Uterine Artery Doppler Measurements154

DiscussionUterine artery Doppler findings within the sec-

ond trimester of pregnancy are thought to havesignificant role in the anticipation of complicationsthat could be seen due to placental failure.Doppler ultrasonography examination has beenused more often recently. It is a noninterventional,simple and repeatable method, which allows theevaluation of blood flow alterations during preg-nancy.5,7

The muscle layer of spiral arteries turns to be afibrinoid structure due to the invasion of trophob-lasts.1 Thus uteroplacental circulation becomes lowresistant. A significant increase in end-diastolic ra-tes, in the later weeks of pregnancy, is seen. Aprogressive decrease in the RI and PI values areobserved due to this low resistant flow.4 EDN, se-en before 24th gestational week, is expected to di-sappear after this week.8

Ther is not a method for the exact anticipationof preeclampsia and IUGR. One of the studies, forthis goal, is Doppler analysis to find out high vas-cular resistance. With Doppler ultrasonographythere have been many surveillance studies in lowand high risk pregnancies.9-12 Presence of differentDoppler indices (high PI, RI values) or EDN havebeen investigated in these studies. Because uterinartery indices may show a large range of variabi-lity due to the location of vessel section studiedand the location of placenta, many researchers cla-im that EDN finding is more convenient ratherthan uterine artery indices.

Hafner et al compared PI and RI values bilat-erally and the presence of EDN between the oneshaving their first and second pregnancies in astudy of 1102 pregnant women who were in the

22th gestational week, and they found no signifi-cant statistical difference.13 They also found thatthe location of placenta did not change Dopplerfindings and that there was no significant statisticaldifference between right and left uterine artery PIand RI average values. In some studies it has beenreported that uterine artery resistance is asymetri-cal, that it has been calculated lower on the sideof placenta, that this difference due to placentallocation disappears after 24th week of gestation.14, 15

It is believed that location of placenta has no effecton uterine artery Doppler findings after 24th week.15

In our study, just like Hafner’s study, we evaluatedPI and RI values of right and left uterine artery sep-arately and reaching the conclusion that there wasno significant statistical difference between bothsides, we used the mean values in the evaluations.

EDN frequency determined in uterine arteriesvaries according to the week of Doppler analysis,ratio of the risky pregnancies in the population.Zimmermann et al found that there was EDN bilat-erally in 8% of 172 low risk pregnancies at the 21-24th weeks, and unilaterally in 12.2 % and in thesame study for the 175 high risk pregnant womenthe ratios were 17.8% and 6.3% respectively.16

Coleman et al reported that there was EDN in 17%of 114 risky pregnant women bilaterally, and 23%unilaterally at the 22-24th gestational weeks. Inaddition Albaiges et al determined EDN bilaterallyin 4.4% of 1757 pregnant women with no risks atthe 23rd gestational week.18 Because placentationhas not been completed yet, Doppler analysisesmade during early weeks of gestation, presence ofEDN is more often.1,4 Murakoshi et al reported thatbilaterally EDN finding with a very high ratio of40.7% at the 18th week decreased to 6.9% in thelater gestational weeks.19 In some studies the pres-ence of EDN seen bilaterally has a range of 3-17%.10,11,18 Harrington et al found that there wasEDN bilaterally in 3.9% of 1326 pregnant womenwith no risks in a surveillance study that tookplace at the 20th and 24th weeks 10. In this studythey also reported that there was EDN bilaterally inthe Doppler ultrasonography examination at the24th gestational week in 55% of the cases who hadpreeclampsia and 18% of the cases with IUGR.

*5th minute Apgar score ≤ 7

Clinical results Group 1 Group 2 P value

(%) (%)

Preeclampsia 3.4 12.2 0.00

IUGR 3.0 9.8 0.04

Low Apgar score* 1.4 7.3 0.03

Preterm delivery 8.4 21.0 0.00

Cesarean rate 16 24 0.15

Tablo 2. Comparison of the perinatal results in Groups 1 and 2.


Albaiges et al evaluated the perinatal outcomesof pregnant women, who came to the hospital forthe routine follow-ups, under the circumstancesthat there was high PI measurements (≥ 1.45) andEDN bilaterally.18 In the presence of EDN, the sen-sitivity for preeclampsia has been reported to be32 %. The sensitivity of fetal death and ablatio pla-centa has been reported to be 83% and 50% res-pectively. Cobian et al studied the relationship bet-ween pathological uterine artery Doppler findings(high RI ratios and diastolic EDN) in the secondtrimester and spontaneous preterm delivery retro-spectively and found that there was no increase inthe risk.20

In a study in our country it has been reportedthat the presence of EDN is more effective than ot-her Doppler findings in the anticipation of probab-le preeclampsia at the 18-26 week.21 Today there isno effective therapy for the prevention of preec-lampsia in the cases having pathological uterine ar-tery Doppler findings during second trimester.6

Though for the close follow-ups for these pregnantwomen, EDN might be a considerable finding.When abnormal Doppler findings are found, moreaggressive approach to the patients and an incre-ase in cesarean section rates are observed 10. Inthis study we also found that the ones with EDN atthe 24th gestational week had higher cesarean sec-tion rates. But there was no significant statisticaldifference between these rates.

ConclusionSurveillance studies of analysis of Doppler

blood flow wave form have gained a great accel-eration during last 10 years owing to tecgnologicalimprovements. Today surveillance studies ofpreeclampsia and/or IUGR in low risk pregnantwomen by using Doppler ultrasonography arecontroversial. There are some conclusions suggest-ing that uterine artery Doppler ultrasonographyexamination is useful only when there is EDN andin low risk pregnant women it is a limited routinesurveillance method 22. In this study it has beenreported that the cases with EDN had an increasedrisk of pregnancy complications, such aspreeclampsia, IUGR, preterm delivery. In low riskpregnancies, predictive value of abnormal Doppler

ultrasonography findings for these complicationsmay be exposed in larger studies.

References

1. Fional L. Development of the utero-placental circulation:The role of carbon monoxide and nitric oxide in trophob-last invasion and spiral artery transformation. MicroscopyResearch and Technique 2003; 60: 402-11.

2. Ohkuchi A, Minakami H, Sato I, Mori H, Nakano T, TatenoM. Predicting the risk of pre-eclampsia and a small-for-ges-tational-age infant by quantitative assessment of the diasto-lic notch in uterine artery flow velocity waveforms in unse-lected women. Ultrasound Obstet Gynecol 2000; 16: 171-8.

3. Prefumo F, Sebire NJ, Thilaganathan B. Decreased endovas-cular trophoblast invasion in first trimestr pregnancies withhigh-resistance uterine artery Doppler indices. Hum Reprod2004; 19: 206-9.

4. Kurjak A, Kupesic S. Doppler sonografi ile erken plasentalgeliflim ve embryonel kan dolafl›m›n›n de¤erlendirilmesi.In: Ertan AK, Tanr›verdi HA (çev Ed). Obstetri ve Jinekolo-jide Renkli Doppler Sonografi, 1. Bask›, Nobel T›p Kitabev-leri, 2003: 109-117.

5. Antsaklis A, Daskalakis G, Tzortz›s E, Michalas S. The effectof gestational age and placental location on the predictionof pre-eclampsia by uterine artery Doppler velocimetry inlow-risk nulliparous women. Ultrasound Obstet Gynecol2000; 16: 635-9.

6. Diagnosis and management of preeclampsia and eclampsia.ACOG Practice Bulletin. Obstet Gynecol 2002; 99: 159-67.

7. Albaiges G, Missfelder-Lobos H, Parra M, Lees C, Cooper D,Nicolaides KH. Comparison of color Doppler uterine arteryindices in a population at high risk for adverse outcome at24 weeks’ gestation. Ultrasound Obstet Gynecol 2003; 21:170-3.

8. Ertan AK, Hendrik HJ, Tanr›verdi HA, Bechtold M, SchmidtW. Fetomaternal Doppler sonography nomograms. ClinExp Obstet Gynecol 2003; 30: 211-6.

9. Bower S, Bewley S, Campbell S. Improved prediction ofpreeclampsia by two-stage screening of uterine arteriesusing the early diastolic notch and color Doppler imaging.Obstet Gynecol 1993; 82: 78-83.

10. Harrington K, Cooper D, Lees C, Hecher K, Campbell S.Doppler ultrasound of the uterine arteries: the importance ofbilateral notching in the prediction of pre-eclampsia, placen-tal abrubtion or delivery of a small-for–gestational–age baby.Ultrasound Obstet Gynecol 1996; 7: 182-8.

11. Harrington KF, Campbell S, Bewley S, Bower S. Dopplervelocimetry studies of the uterine artery in the early predic-tion of pre-eclampsia and intra-uterine growth retardation.Eur J Obstet Gynecol Reprod Biol 1991; 4: 14-20.

12. Valensise H, Bezzeccheri V, Rizzo G, Tranquilli AL, Garzet-ti GG, Romanini C. Doppler velocimetry of the uterine ar-tery as a screening test for gestational hypertension. Ult-rasound Obstet Gynecol 1993; 3: 18-22.

13. Hafner E, Schuchter K, Metzenbauer M, Phlipp K. Uterineartery Doppler perfusion in the first and second pregnan-cies. Ultrasound Obstet Gynecol 2000; 16: 625-9.

14. Fleischer AC, Manning FA, Jeanty P, Romero R. SonographyIn Obstetrics And Gynecology. 5th ed. New-York, App-leton&Lange; 1996; p: 229-234.

Yaz›c› FG et al., Relationship of Early Diastolic Notch in Uterine Artery Doppler Measurements 156

15. Kofinas AD, Penry M, Simon NV, Swain M. Interrelations-hip and clinical significance of increased resistance in theuterine arteries in patients with hypertension or preeclamp-sia or both. Am J Obstet Gynecol 1992; 166: 601-6.

16. Zimmermann P, Eirio V, Koskinen J, Kujansuu E, Ranta T.Doppler assessment of the uterine and uteroplacental cir-culation in the second trimestr in pregnancies at high riskfor pre-eclampsia and/or intrauterine growth retardation:comparison and correlation betweeen different Dopplerparameters. Ultrasound Obstet Gynecol 1997; 9: 330-8.

17. Coleman MA, McCowan LM, North RA. Mid-trimestir uter-ine artery Doppler screening as a predictor of adverse preg-nancy outcome in high-risk women. Ultrasound ObstetGynecol 2000; 15: 7-12.

18. Albaiges A, Missfelder-Lobos H, Lees C, Parra M, NicolaidesKH. One-stage screening for pregnancy complications bycolor Doppler assessment of the uterine arteries at 23week’s gestation. Obstet Gynecol 2000; 96: 559-64.

19. Murakoshi T, Sekizuka B, Takakuwa K, Yoshizawa H,Tanaka K. Uterine and spiral artery flow velocity wave-forms in pregnancy-induced hypertension and/or int-rauterine growth retardation. Ultrasound Obstet Gynecol1996; 7: 122-8.

20. Cobian-Sanchez F, Prefumo F, Bhide A, Thilaganathan B.Second-trimestur uterine artery Doppler and spontaneouspreterm delivery. Ultrasound Obstet Gynecol 2004; 24:435-9.

21. Donduran S, Yoldemir T, fienda¤ F, Özbek S, Gündem G,Özk›nay E ‹kinci trimester uterin arter ve fetal orta serebralarter doppler ölçümlerinin intrauterin geliflme gerili¤i vepreeklampsi gelifliminde prediktif de¤eri. Klinik Bilim-ler&Doktor 2002; 8; 764-70.

22. Heybeli SG, Dede FS, Dede H, Aykan B, Köse F. Preek-lampsi ve intrauterin geliflme gerili¤inin erken tahminindeuterin ve umbilikal arter doppleri. Türkiye KlinikleriJinekoloji Obstetrik 2002; 12: 116-20.



AbsractObjective: To evalute the pregnancies with polyhydramnios who had delivered in our clinics and matched with control groupretrospectively.

Methods: Ninety five pregnancies with polyhydramnios (group 1) delivered were evaluated retrospectively and ninety five preg-nancies delivered spontaneously were chosen randomly as control group (group 2) between January 1998 and June 2004 atObstetrics Department. The demographic characteristics, maternal age, delivery modes, neonatal weight, apgar scores, cesare-an rates and indications, fetal anomalies, perinatal mortality rates were evaluated for each group. Student –t and Chi-squre testswere used for statatistical analyses.

Results: The mean age of group 1 was 29.72±7.34 and group 2 was 30.74±2.01 (p>0.05). Prevalance rate of polyhydramni-os was 1.01%. The etiology of polyhydramnios was seen as idiopathic causes 41 (43.15%), Central nervous system anomalies21 (22.10%), gastrointestinal system anomalies 10 (10.52%), diabetes mellitus 8 (8.42%), hydrops fetalis 7 (7.36%), other fe-tal causes 7 (7.36%), twin-to-twin transfusion syndrome 1 (1.05%). Twenty three cases (24.21%) had preterm labour, 11(11.57%) cases were twin pregnancy in polyhydramnios group. Cesarean section rate was 35 (36.84%) in group 1 and 44(46.31%) in group 2 (p>0.05). The most common cesarean endication was fetal distress (11.57%) in group 1 and previous ce-sarean in group 2 (21.19%). Median birth weight was 2224 ± 1219 in group 1 and 3414 ± 521 in group 2 (p<0.001). Fetal ano-maly rate was 37.89% in group and 3.15% in group 2 (p<0.001). Perinatal mortality rate was 54.73% in group 1 and 6.31%in group 2 (p<0.001). 1st minutes apgar score was 3.2 ± 2.7 and 5th minutes apgar score was 3.8±3.8 in group 1 and 1st min-utes apgar score was 7.09 ± 1.5 and 5th minutes apgar score was 8.8±1.9 in group 2 (p<0.001).

Conclusion: Although the common seen etiologies of polyhydramnios were idopathic and central nervous system, preventab-le causes of polyhdramnios such as Rh isoimmunisation and diabetes mellitus also plays important role in the etilogy of polyhyd-ramnios. Improvement of antenatal care services might reduce preventable causes of polyhdramnios. Termination of anomaliessuch as anencephaly at early gestasional week reduces maternal risks and economical loss.

Keywords: Polyhydramnios, etiology, fetal anomaly.

Polihidramnios olgular›n›n retrospektif analizi

Amaç: Klini¤imizde do¤umu gerçekleflen polihidramnios olgular›n›n retrospektif analizini yapmak ve kontrol grubu ile karfl›lafl-t›rmakt›r.

Yöntem: Ocak 1998 ile Haziran 2004 tarihleri aras›nda klini¤imizde do¤um yapan 95 polihidramnios olgusundan grup1, ayn›dönemde miad›nda do¤um yapan ve randomize seçilen 95 normal olgudan grup 2 oluflturuldu. Her iki grubun anne yafllar›, do-¤um flekilleri, do¤um a¤›rl›klar›, APGAR skorlar›, sezaryen oran› ve endikasyonlar›, fetal anomaliler ve perinatal mortalite aç›s›n-dan retrospektif olarak analiz edildi. ‹statistiksel analizlerde student t ve ki-kare testleri kullan›ld›.

Bulgular: Grup 1 olgular›n›n ortalama yafl› 29.72±7.34 ve grup 2’nin ise 30.74±2.01 olarak bulundu (p>0.05). Ayn› dönemdepolihidramnios tüm gebelikler içerisinde %1.01 oran›nda bulundu. Polihidramnios etiyolojisinde s›kl›k s›ras›na göre; idiopatik 41(%43.15), santral sinir sistemi lezyonlar› 21 (%22.10), gastrointestinal sistem anomalileri 10 (%10.52), diabetes mellitus 8

Retrospective Analysis of PolyhydramniosCases

Ahmet Kale, Nurten Akdeniz, Mahmut Erdemo¤lu, Ahmet Yal›nkaya, Murat Yayla

Department of Gynecology and Obstetrics, Faculty of Medicine, Dicle University, Diyarbak›r

Correspondence: Dr. Ahmet Kale, Dicle Üniversitesi T›p Fakültesi, Kad›n Hastal›klar› ve Do¤um Anabilim Dal›, 21280 Diyarbak›re-mail: [email protected]

Introduction Polyhydroamnios is defined as the recruitment

of 2000 ml or more amniotic fluid.1 the presence of500-2000 ml amniotic fluid at term is accepted asnormal. It is also defined as the width of amnionfluid pouch being more then 8 cm in ultrasono-grapy or the amnion fluid index being more than95% for gestational age or the amount of amnioticfluid, amniotic fluid index (AFI) is calculated bythe addition of the vertical depth of the biggestpouch in the four equal quadrants. In a 26-39week pregnancy the upper border of AFI is greaterthan 24 cm. Polyhydroamnios is seen in 1-3.2% ofpregnancies.2 Perinatal morbidity and mortalityincrease with polyhydroamnios. In polyhydroam-nios, the frequency of congenital abnormalitiesincreases but the ratios of chromosome abnormal-ities differ between studies for some unknown rea-son.3

In this study cases who had attended our clin-ic because of polyhydroamnios and had deliverywere investigated retrospectively with respect tomaternal and fetal characteristics.

MethodsA total of 95 polyhydroamnios cases who had

deliveries in the 6 year period between January1998 and June 2004, at Dicle University Faculty ofMedicine Department of Obstetrics and Gynecologywere studied retrospectively. All the information

about the cases were obtained from the computerand folder data. Ages of the mothers, the proce-dure of delivery, birth weights, APGAR scores, cae-sarian ratios and indications, fetal anomalies wereevaluated retrospectively for perinatal mortality. 95cases who had deliveries because of polyhy-droamnios were taken as Group 1, 95 cases whoattended the clinic at the same time interval forterm pregnancies and had deliveries were taken asgroup 2 (the control group). Both groups wereevaluated retrospectively for procedure of deliv-ery, birth weights, APGAR scores, fetal anomaliesand perinatal mortality.

The results were evaluated by student-t test andchi square test and SPSS 11.0 statistical programwere used, p<0.05 were accepted as statisticallysignificant.

Results95 cases who had deliveries with the diagnosis

of polyhydroamnios between January 1998 andJune 2004 were found. A total of 9318 deliverieswere performed in our clinic during this time peri-od. The ratio of the pregnant women who haddeliveries with the diagnosis of polyhydroamniosto all of the deliveries was 1.01%. The greatest per-centage of our cases were idiopathic polyhy-droamnios 43.15% (n=41). The second greatestcause was fetal abnormalities 37.89% (n=36),among fetal abnormalities central nervous systemabnormalities were the commonest. Among the

(%8.42), immun hidrops fetalis 7 (%7.36), di¤er fetal nedenler 7 (%7.36) ve ikizden ikize transfüzyon sendromu 1 (%1.05) ol-guda saptand›. Olgular›n 23 (%24.21)’unda preterm eylem, 11 (%11.57)’inde ikiz gebelik saptand›. Grup 1’de 35 (%36.84) ol-guda, grup 2’de ise 44 (%46.31) olguda do¤um sezaryen ile gerçekleflti (p>0.05). En s›k sezaryen endikasyonu grup 1’de fetaldistres (%11.57), grup 2 ise eski sezaryen (%21.19) saptand› (p>0.05). Grup 1 olgular›nda neonatal a¤›rl›k 2224 ±1 219 g vegrup 2’de 3414 ± 521 g bulundu (p<0.001). Fetal anomali grup 1’de %37.89, grup 2’de %3.15 oran›nda bulundu (p<0.001).Perinatal mortalite grup 1’de %54.73, grup 2’de ise %6.31 oran›nda bulundu (p<0.001). Grup 1 olgular›nda 1. dakika APGARskoru 3.2 ± 2.7 ve 5. dakika 3.8 ± 3.8, grup 2’de ise 7.09±1.5 ve 8.8 ± 1.9 olarak bulundu (p<0.001).

Sonuç: Çal›flmam›zda etyolojik faktörler aras›nda en s›k idyopatik ve santral sinir sistemi anomalileri saptan›rken antenatal önle-nebilen immünize Rh ve Diabetes Mellitus gibi sebepler de önemli yer tutmaktad›r. Antenatal bak›m hizmetlerinin artt›r›lmas› ön-lenebilir etiyolojik faktörleri azaltabilir. Ayn› zamanda yaflamla ba¤daflmayan anensefali gibi anomalilerin erken gebelik haftala-r›nda sonland›r›lmas› maternal riskleri azalt›r ve daha az ekonomik kayba neden olur.

Anahtar Sözcükler: Polihidramnios, etyoloji, fetal anomali.


chromosomal causes of polyhydroamnios, Downsyndrome was present in 2 (%2.1) cases. In 8(%8.42) of the cases because of Rh immunizationand in 1 (%1.05) because of non immune reasonshydrops had developed. DM was found in 7 of thepolyhydroamnios cases (7.36%) (Table 1). Pretermdelivery because of polyhydroamnios preterm23(%24.21) and twin pregnancy were found in 11(%11.57) cases.

When both groups were compared the averageage of group 1 was 29.72 ± 7.34, of group 2 was30.74 ± 2.01 (p>0.05). In group 1 in 35 (%36.84)cases, in group 2 in 44 (%46.31) cases had caesa-rian (p>0.05). In polyhydroamnios cases caesarianbecause of fetal distress was in the first line(%11.57).

The average birth weight of the babies belong-ing to group 1 was (2224 ± 1219 g.) and was lowerthan that of group 2 (3414 ± 521 g.) (p<0.001).Fetal abnormality ratios in group 1 cases was(%37.89) and were apparently higher than group 2(%3.1) (2 hydrocephalus, 1 achondroplasia)(p<0.001). The perinatal mortality ratios in group 1cases (%54.73) were apparently higher than that ofgroup 2 (%6.31). First and 5th minute APGAR scoreswere higher in group 2 cases (p<0.001).

DiscussionAmniotic fluid normally is estimated to be 200

ml at 16th week, 1000ml at 28th week, 900 ml at 28thweek and 800 ml at 40th week. Generally polyhy-droamnios is seen in 1-3.25 of pregnancies.2

Incidence of polyhydroamnios were reported as%0.4 by Queenan et al,1 %3.3 by Chamberlain etal.3 in our cases polyhydroamnios was seen %1.01in accordance with literature.

Amniotic fluid volume changes during preg-nancy; is controlled by dynamic relations betweenmaternal, fetal and placental compartments.4 Whenthe balance between these compartments are lostthe pregnancy is under risk.5 The most frequentreason for polyhydroamnios is idiopathic.6 In astudy conducted on 149 patients Golan et al7 foundthe cause in 2/3 of the patients to be idiopathic. Inour study group the reason of polyhydroamnioswas found to be idiopathic in 41 cases (%43.15).

In Rh immunization and fetal hydrops casespolyhydroamnios may be seen secondary toincreased cardiac output. In fetuses with Rh immu-nization and fetal hydrops it has been shown thatlactate concentration increases secondary tohypoxia and this increase in lactate creates anosmotic effect and moves the fluid in fetal com-partment to maternal compartment.8 In our studygroup polyhydroamnios secondary to fetalhydrops were seen in 9 (%9.47) cases; 7 of thesehydrops fetalis cases were caused by immune and2 were by nonimmune causes.

Polyhydroamnios accompanies fetal malforma-tions especially central nervous system or gastroin-testinal anomalies.9,22 in a study conducted byCarlson et al.10 fetal anomaly rates were found tobe 44% in cases with polyhydroamniosis. In ourstudy group fetal abnormalities were detected in36 cases (%37.89) and this ratio was apparentlyhigher than that of the control group (p<0.001). Inpolyhydroamniosis cases abnormalities encoun-tered most frequently were central nervous systemabnormalities and gastro intestinal system abnor-malities were in the second line. Among centralnervous system abnormalities anencephaly wasthe most frequent abnormality with 13 cases(%13.68). Problems in fetal swallowing in anen-cephaly, transudation of fluid from the meningesor polyuria as a result of vasopressin deficiencymay cause increase in the amount of the amnionfluid.11

n %

1. Idiopathic 41 43.15

2. Diabetes mellitus in mother 8 8.42

3. Reasons belonging to the fetus

a. Central nervous system lesions 21 22.10

1. Anencephalicus 13 13.68

2. Hydrocephalicus 5 5.26

3. Spina bifida 2 2.10

4. Encephalocel 1 1.05

b. Gastrointestinal system abnormality 10 10.52

1. Esophageal atresia 5 5.26

2. Duodenal atresia 4 4.21

3. Anus imperforates 1 1.05

c. Immune hydrops fetalis 7 7.36

d. Down syndrome 2 2.10

e. Non-immune hydrops fetalis 2 2.10

f. Skeletal displasia 1 1.05

g. Cystic higroma 1 1.05

h. Epidermolisis bullosa 1 1.05

4. Feto-fetal transfusion syndrome 1 1.05

Table 1. Factors in the etiology of polyhydroamniosis.

Kale A et al., Retrospective Analysis of Polyhydramnios Cases160

Polyhydroamnios may be accompanied bychromosomal abnormalities. Brady et al12 foundthe rate of fetal trisomy in the idiopathic polyhy-droamnios group as %3.2. Landy et al13 in theirseries with 59 patients determined the rate of chro-mosomal abnormalities to be %1.7. the rate ofchromosomal abnormalities in our cases werefound to be %2.1 (2 trisomy 21).

Amniotic fluid problems and especially polyhy-droamnios may be seen %12 in twin pregnan-cies.14,23 In our study there were 11 twin pregnancycases (%11.57). Feto-fetal transfusion was presentin one. In feto-fetal transfusion syndrome it wasshown that the acceptor fetus is polyuric, dilatedglomeruli and distal collecting tubules were detect-ed histologically and increase in cardiac outputwas shown in these cases.15

In maternal diabetes secondary polyhydroam-nios incidence may be between %5-13. Fetalpolyuria secondary to osmotic diuresis may causepolyhydroamnios in diabetes.11 in our study grouppolyhydroamniosis related to diabetes was seen in8 cases (%8.42).

One of the important maternal and fetal com-plications of polyhydroamnios is preterm laborand the risks caused by the labor.16 In a study con-ducted by Many et al21 preterm labor rate in 275polyhydroamnios cases were found to be %18.9.In our study group preterm labor because of poly-hydroamniosis was detected in 23 cases (%24.21).

Perinatal mortality rate in polyhydroamniosvaries between %10 and %30.17 In a study con-ducted by Sickler et al18 in their polyhydroamniosseries of cases, perinatal mortality ratio was foundto be %39. The ratio of perinatal mortality relatedto polyhydroamnios in our series was found to be%54.73 and this ratio was significantly higher thanthe control group (p<0.001). In cases with polyhy-droamnios 1st and 5th minute APGAR scores andthe average birth weights of the newborns (2224 ±1219), were apparently lower in the control group(p<0.001). this apparently high perinatal mortalitylevel may be related to the high congenital mal-formation and preterm delivery ratios, low APGARscore in the newborn and low average birthweight in polyhydroamnios cases. The fact that weare a referral center for the follow up and treat-ment of high risk pregnancies in our region con-

tributes to the high mortality and morbidity ratiosin our cases with polyhydroamniosis.

Caesarian delivery is increased in cases withpolyhydroamnios.19 In 35 of our cases caesarianwas performed (%36.84) and caesarian because offetal distress was in the first line (%11.5). The cae-sarian group when compared with the controlgroup was not statistically significant (p>0.05). Thissituation may be explained by the high level ofcaesarians performed in our region.20

In conclusion; when poyhydroamnios is detect-ed, the cases should be examined for fetal centralnervous system and gastrointestinal system abnor-malities, Rh immunization, and maternal diabetesmellitus. Necessary medical preventions must beperformed to prevent preterm labor and fetal mor-bidity and mortality.

References

1. Queenan JT, Gadow EC. Polyhydramnios: Chronic versusacute. Am J Obstet Gynecol 1970; 108: 349-55.

2. Fisk NM, Moessinger AC. Oligohydramnios and polyhyd-ramnios. In: Reed GB, Claireaux AE (eds), Diseases of thefetus and newborn, (2.ed), London: Chapman and Hall,1995: 1243.

3. Chamberlain PF, Manning FA, Morrison I, Harman CR, Lan-ge IR. Ultrasound evaluation of amniotic fluid volume.Therelationship of marginal and decreased amniotic fluid volu-mes to perinatal outcome. Am J Obstet Gynecol 1984; 150:245-9.

4. Chescheir NC, Seeds JW: Polyhydramnios and oligohyd-ramnios in twin gestations. Obstet Gynecol 1988; 71: 882-4

5. Goldstein RB, Filly RA. Sonographic estimation of amnioticfluid volume. Subjective assessment versus pocket measu-rements. J Ultrasound Med 1988; 7: 363-9.

6. Hill LM, Breckle R, Thomas ML, Fries JK. Polyhydramnios:ultrasonically detected prevalence and neonatal outcome.Polyhydramnios: ultrasonically detected prevalence and ne-onatal outcome. Obstet Gynecol 1987; 69: 21-5.

7. Golan A, Wolman I, Saller Y, David MP. Hydramnios insingleton pregnancy: sonographic prevalence and etiology.Gynecol Obstet Invest 1993; 35: 91-3.

8. Soothill PW, Nicolaides KH, Rodeck CH, Clewell WH, Lind-ridge J. Relationship of fetal hemoglobin and oxygen con-tent to lactate concentration in Rh isoimmunized pregnan-cies. Obstet Gynecol 1987; 69: 268-71.

9. Özgünen F, Evrüke C. Hidramnios ve Oligohidramnios.Beksaç S . Maternal – Fetal T›p ve Perinatoloji. 1. bask›. An-kara, Nobel; 2001; 1132-41.

10. Carlson DE, Platt LD, Medearis AL, Horenstein J. Quan-tifiable polyhydramnios: diagnosis and management.: Obs-tet Gynecol 1990; 75: 989-93.

11. Teoh TG, Fisk NM. Hydramnios, oligohydramnios. In:James DK, Ster PJ, Weiner CP, Gonik B(eds). High Riskpregnancy, North Yorkshire: WB Saunders, 1999: 309.


12. Brady K, Polzin WJ, Kopelman JN, Read JA. Risk of chro-mosomal abnormalities in patients with idiopathic polyhyd-ramnios. Obstet Gynecol 1992; 79: 234-8.

13. Landy HJ, Isada NB, Larsen JW Jr. Genetic implications ofidiopathic hydramnios. Am J Obstet Gynecol 1987; 157: 114-7.

14. Koç A. Ço¤ul Gebelikler. Beksaç S. Maternal – Fetal T›p vePerinatoloji. 1. bask› Ankara, Nobel; 2001; 1122-31.

15. Naeye Rl, Milic AMB, Blane W. Fetal endocrine and renaldisorders: clues to the origin of hydramnios. Am J ObstetGynecol 1979; 108: 1251-6.

16. Clark Sl, De Vore GR. Prenatal diagnosis for couples whowould not considerabortion. Obstet Gynecol 1987; 157: 114-7.

17. Carlson DE, Platt LD, Medearis AL, Horenstein J. Quan-tifiable polyhydramnios: diagnosis and management. ObstetGynecol 1990; 75: 989-93.

18. Sickler GK, Nyberg DA, Sohaey R, Luthy DA. Polyhydram-nios and fetal intrauterine growth restriction: ominous com-bination. J Ultrasound Med 1997; 16: 609-14.

19. Jacoby HE, Charles D. Clinical conditions associated withhydramnios: Am J Obstet Gynecol 1966; 94: 910-9.

20. Yal›nkaya A, Bayhan G, Kale A, Yayla M. Dicle Üniver-sitesinde 20 Y›ll›k Sezaryen Oran› ve Endikasyonlar›: T KlinJinekol Obstet 2003; 13: 356-60.

21. Many A, Hill LM, Lazebnik N, Martin JG. The associationbetween polyhydramnios and preterm delivery. ObstetGynecol 1995; 86, 389-91.

22. Volante E, Gramellini D, Moretti S, Kaihura C, BevilacquaG. Alteration of the amniotic fluid and neonatal outcome.Acta Biomed Ateneo Parmense 2004; 75, 71-5.

23. Orhan A, Kurzel RB, Istwan NB, Rhea D, Burgess E, Stan-ziano G. The impact of hydramnios on pregnancy outcomein twin gestations. J Perinatol 2005; 25: 8-10.

Kale A et al., Retrospective Analysis of Polyhydramnios Cases162

Abstract

Backround: To discuss the diffuculties in the diagnosis of meconium peritonitis and to determine the role of magnetic reso-nance in differential diagnosis.

Case: Twentyfour-year-old woman with a 33-gestational-weeks pregnancy was hospitalized due to polyhydramnios and a fetalpelvic semi-solid mass with areas of calcifications, measuring 66x55 mm in diameter, showing no vascularization that was diag-nosed by obstetric ultrasonography, magnetic resonance and fetal Doppler imaging. Antenatal diagnosis of a type 4 sacrococ-cygeal teratoma turned out to be meconium ileus-peritonitis during postpartum laparotomy and cystic fibrosis was final diag-nosis.

Conclusion: When an intraabdominal mass is seen in a fetus with ultrasonograghy and magnetic resonance, especially accom-panied by ascites, intraabdominal calcifications and bowel dilatations, meconium peritonitis and ileus should be considered inthe differential diagnosis.

Keywords: Meconium peritonitis, sacrococcygeal teratoma, magnetic resonance.

Prenatal sakrokoksigeal teratom tan›s› alm›fl bir mekonyum ileus-peritonit olgusu

Amaç: Mekonyum ileus tan›s›ndaki zorluklar ve tan›da fetal manyetik rezonans görüntülemenin yerini tart›flmak.

Olgu: Yirmidört yafl›nda, 33 hafta 3 günlük tekil gebeli¤i mevcut hastada, obstetrik ultrasonografi, manyetik rezonans ve fetalDoppler incelemelerinde, fetal pelvis yerleflimli, 66x56 mm boyutlar›nda, semisolid, yer yer kalsifikasyonlar içeren, vaskülarite gös-termeyen kitle ve polihidramnios saptanmas› üzerine hospitalize edilmifltir. Bu antenatal incelemeler sonucu tip 4 sakrokoksige-al teratom öntan›s› alan fetus, do¤umu takiben yap›lan laparotomi s›ras›nda mekonyum ileus–peritonit olarak de¤erlendirilmiflve ileri tetkiklerde kistik fibrozis saptanm›flt›r.

Sonuç: Ultrasonografi ve manyetik rezonans görüntüleme fetusta bat›nda kitle izlenmesi halinde, özellikle de asit, intraabdomi-nal kalsifikasyon, barsak dilatasyonu gibi bulgular efllik ediyorsa mekonyum ileusu ve peritoniti ay›r›c› tan›da düflünülmelidir.

Anahtar Sözcükler: Mekonyum periteniti, sakrokoknigeal teratoma, magnetik rezonans.


A Case Report of Meconium Ileus-Peritonitis witha Prenatal Diagnosis of Sacro-Coccygeal Teratoma

Baflak Baksu1, ‹nci Davas1, Jale Özgül1, Figen Ezen1, Alper Özel2, Gülden Yenice2, Mehmet Yalç›n3

1Clinics of Gynecology and Obstetrics, 2Department of Radiology, 3Clinics of Pediatric Surgery, fiiflli Etfal Hospital, ‹stanbul

Correspondence: Dr. Baflak Baksu, fiiflli Etfal Hastanesi, Kad›n Hastal›klar› ve Do¤um Klini¤i, ‹stanbul, e-mail: [email protected]

Backround

In gynaecology there have been many

improvements about congenital anomalies during

last 20 years. The main cause of this improvement

is the common usage of obstetric ultrasonography.Determination of constitutional anomalies by ultra-sonography is about 70%. Thus antenatal controlbecomes more important.1 Accurate diagnosis ofgastrointestinal system anomalies, just like consti-

tutional ones, is closely associated with postnataloutcomes becuse of better birth planning, earlysurgical intervention, fewer complications.

Ultrasonography is essential for the diagnosis ofgastrointestinal system anomalies. The most oftenfindings of these anomalies are dilation of bowels,polyhydramnios, hyperechogenic bowel andascites. Most of these findings are not specific, theycan arise lately during pregnancy and they may bedue to temporary variations.2 The sensitivity ofobstetric ultrasonography to designate these anom-alies depend on the specific characteristics of theanomaly itself.3 During recent years some groupssuggested using magnetic resonance (MR) for thedetermination of gastrointestinal anomalies orimaging the normal bowel adjacent to the intraab-dominal cyst.4

In our article a case, which had been diagnosedas type 4 sacrococcygeal teratoma by ultrasonog-raphy and obstetric MR but which appeared to bemeconium ileus-peritonitis peroperatively, hasbeen presented. Difficulties in the diagnosis ofmeconium ileus and the place of fetal MR imaginghas been discussed.

CaseA 24 year old woman, who gave two vaginal

births, who had an operation of ectopic pregnan-cy applied. She had a pregnancy, one fetus, of 33weeks and 3 days according to her LMD. After sec-ond level ultrasonography and Doppler examina-tion a semisolid mass, localized adjacent to fetalpelvis, having 66x56 mm dimensions, containingsome calcifications, having no vascularization andpolyhydramnios were seen. Sacrococcygeal ter-atoma was the prediagnosis. The patient did nothave a history of birth with a congenital anomaly.But first degree relative marriage was present(cousins). Obstetric examination findings were:collum was dilated (2 cm), no effacement, headfirst, head was mobile, pouch was intact.According to obstetric ultrasonography intrauter-ine, alive, one fetus was present. Biparietal diame-ter was 82 mm, head circumference was 301 mm,abdomen circumference was 330 mm, femurlength was 65 mm. Amniotic liquid index was 40cm and the placental location was the front wall.In the fetus pelvis a septate mass between urinebladder and columna vertebralis with dimensions55x70 mm, with heterogeneous echogenicity andcalcifications was seen, coexistent with ascites inthe abdomen (Figure 1).

Baksu B et al., A Case Report of Meconium Ileus-Peritonitis with a Prenatal Diagnosis of Sacro-Coccygeal Teratoma164

Figure 1. In the fetal pelvis a calcified,septate mass with dimensions of 55x70 mm, with heterogeneous echogenicity. Also ascites in abdomen.


With these findings the patient was sent toRadiology department for obstetric MR imaging.Obstetric MR imaging was made within a 1.5 Tesla(Signa; GE Medical Systems, Milwaukee,Winconsin) MR machine by using body-coil. Thefetal position was determined by sonography.Neither maternal premedication nor contrast agentwere used for fetal sedation. The images wereobtained at axial, coronal and sagittal planes, withHalf-Fourier Single Shot Turbo Fast Spin Echo T1and T2w sequences. Space occupying lesion, fill-ing fetal pelvis and abdomen, consisting of solidcomponents but cystic structure predominantlywas measured 60x70 mm. The extension of thelesion lead to presacral area. At the T2w sequencescystic components appeared to be hyperintense, atthe T1w sequences they appeared to have hypo-intermediate intensity. Hypointense foci wereaccepted to be calcifications. Ascites and anincrease in the amnios liquid amount in fetalabdomen were coexistent (Figures 2 and 3 ). Fetalstomach, duodenum and the jejunal loops seemedto have normal diameters (Figure 4). The lumen ofrectum seemed to be patent and colon segmentscould not be visualized. It was thought to be dueto the compression of the lesion. Mild dilation inthe collecting system of fetal kidneys was owingto the distal compression (Figure 5). It was thought

that with the MR findings the space occupyinglesion, filling fetal pelvis-presacral area andabdomen, consisting of solid components but cys-tic structure predominantly, was a sacrococcygealteratoma with an intraabdominal location (type 4according to American Academy of Pediatrics).5

Following examinations were suggested.

At the follow-ups it was seen that the amountof ascites increased. Contractions began at the 20th

day of hospitalization. Because the actualapproach for the type of birth depends on thedimensions of the tumor (mass > 5cm), the birthtook place by cesarean section 1. She gave birth toa girl, 49 cm, 3400 gr, and the first minute APGARscore was 8. The newborn and pediatric surgerygroups examined her. Their findings were: heartapex rate 140/min, cardiovascular and respiratorysystem examinations were normal. There wasabdominal distension and mild venous dilation.There were no bowel sounds by oscultation, anuswas open and no meconium was seen at rectaltouch. There was gas image, filling half of theabdomen, and levels in the plain abdomen radi-ogram. At first meconium ileus and peritonitis,pouch colon, colonic atresia and aganglionicmegacolon was considered. The baby had anoperation 36 hours after birth. At laparotomy, all ofthe bowel walls and the omentum were covered

Figures 2 and 3. Sagittal and coronal images show septate structures, cystic predominant space occupying lesion with a solidcontent, hypointense calcification on the septa, fetal ascites, polyhydramnios.

by cystic meconium. Omentum was necrotic andadhered to abdominal wall. There were adhesions.Necrotic omental structures and adhesions wereexcised. Many loculated cystic structures (meconi-um cysts) were excised and aspirated. Ascendingcolon and ileum formed a mass in the form ofvolvulus. There was ileal perforation 40-50 cmbefore the ileocecal valve and the distal parts fromhere were filled with meconium plug untill sig-moid colon. Meconium was decompressed manu-ally to the proximal parts and was cleaned.Loopostomy to the skin was applied at this area inthe right lower quadrant. So meconium ileus pre-diagnosis was confirmed. Biopsy taken from thedistal part showed us the presence of ganglioniccells, which eliminated the diagnosis “aganglionicmegacolon”. ‹leostomy was closed 2 months later.She was found to have cystic fibrosis, usuallyaccompanied by meconium ileus, after advancedstudies had been made. The baby is now 9 monthsold, weighs 5600 gr and goes on to have therapy.

DiscussionMeconium peritonitis is a rare, fetal and neona-

tal condition. It especially takes place after antena-tal bowel perforation, involving small bowel.2

Ileum perforated 40-50 cm before the ileochecal

valve in our case. Although predispositions areatresia of small bowels, meconium ileus, volvulusand intussusception, mostly it is idiopathic.6

Ascending colon and ileum formed a mass in theform of volvulus in our case. Meconium peritonitisis classified into three groups; massive generalizedperitonitis (type 1), meconium pseudocyst (type2), prenatal total restoration resulting in residualintraabdominal calcification (type 3). Prognosis isvariable and mostly depends on the predisposingpathology and coexistent anomalies.7 Prognosis isbetter in the cases of meconium peritonitis withoutgastrointestinal malformation.8 In our case meconi-um ileus was accompanied by volvulus in theascending colon and ileum.

Although meconium ileus and peritonitis canbe diagnosed by ultrasonography, findings arevariable. Prenatal sonographic imaging can be sup-ported by findings such as bowel obstruction,meconium pseudocyst, intraperitoneal calcifica-tions, fetal bowel dilation, sometimes by polyhy-dramnios or fetal hydrops. There may only be theimage of fetal ascites.7 The most typical antenatalultrasonographic finding is intraperitoneal calcifi-cations. These calcifications form owing to inflam-matory reaction stimulated by intraperitonealmeconium and resulting in the calcification offibrous tissue.6 When an intraabdominal echogenic


Figure 4. Coronal image shows bowel loops with normal cal-ibration close to the space occupying lesion.

Figure 5. Axial image shows the space occupying lesion anddilation in the renal collecting system bilaterally.

cyst is seen, meconium pseudocyst must be con-sidered for differential diagnosis. After perforation,the bowel content, that spreads into the abdomen,is surrounded by bowels and a fibrous tissue formsaround it. This pseudocyst has an irregular andthick wall and may contain debris, septations, cal-cification or all of them.7 There was a mass with aheterogeneous echogenicity, septations and calcifi-cation and ascites in the abdomen in our case.

Incidence of sacrococcygeal teratoma is1/40000 and it is the most often seen fetal neopla-sia. It may also have similar imaging charasteristics.It originates from presacral area. Depending on theextension to pelvis and abdomen, it is classifiedinto 4 groups. Type 4 is an internal mass with noexternal component. Its frequency is 10% amongall teratomas. 85% of sacrococcygeal teratomascontain solid-cystic mixed forms. Calcification maybe seen in 2/3 of the cystic lesions with a thickwall and containing solid components. It is usual-ly accompanied by polyhydramnios. It may beseen with placentomegaly and fetal hydrops. MR isuseful in determining the dimensions of the lesionand the abdominal, especially intrapelvic exten-sion of the lesion.9,10

Meconium pseudocyst and sacrococcygeal ter-atoma may have similar imaging charasteristics.Lesion with cystic-solid components, calcified con-tent, polyhydramnios and hydrops may be seen inboth conditions. Dilated bowels may also be seenin both meconium ileus-peritonitis and in the con-dition of being secondary to compression effect ofthe mass. In both cases proximal bowels may havenormal width and normal imaging charasteristics.At MR imaging cystic content appears hyperin-tense in T2w sequences, in T1w sequences itappears in intermediate intensity, in sacrococ-cygeal teratoma it may appear hypointense or haveintermediate signal intensity compared to cysticcontent.

In our case of 33 week gestational age thelesion was of mixed structure and contained solid-cystic components. The cystic areas appearedhypoechoic at ultrasonography. MR imagingrevealed proximal jejunal loops with normal widthand no dilated bowel loops. Sonography revealedno echogenic bowel appearance. In fetal abdomenthere was free peritoneal fluid and dilation of renalcollector system secondary to compression bilater-

ally. With these findings, the prenatal diagnosis ofour case was type 4 sacrococcygeal teratoma aftersecond level ultrasonography, fetal Doppler andMR imaging modalities were applied. If ultra-sonography follow-ups of the pregnant womanhad been made properly, dilated-echogenic bowelloops could have been seen earlier and with MRimaging location of obstruction and loops havingabnormal signal characteristics could have helpeddiagnose meconium ileus. Dilated bowels withmeconium can be shown at about 27th week;meconium pseudocyst arises about 32nd week.9

Veyrac et al studied fetal gastrointestinal systemanomalies with MR. They saw that meconiumpseudocyst had fluid-like signal in T2w sequencesand had intermediate signal intensity in T1wsequences. So they can be differentiated fromsome other cysts such as duplication cysts.2 All ofintraabdominal cystic masses should be taken intoconsideration for differential diagnosis. Amongthese, sacrococcygeal teratoma, which is the mostoften fetal neoplasia, is the leader.12 Intraperitonealcalcifications accompanying a complicated cysticmass make the diagnosis easier.6

Although Clatworthy defines meconium ileus asa separate condition, he/she and other researchershave reported that this condition could be the firstfinding of aganglionic megacolon or cystic fibro-sis.2 The diagnosis of aganglionic megacolon waseliminated after peroperative biopsy. Postoperativeadvanced studies revealed the diagnosis of cysticfibrosis.

Many studies have been made for showing thecorrelation between the prenatal findings of meco-nium ileus and peritonitis and newborn out-comes.7,13,14 Eckoldt et al determined a probablegastrointestinal system anomaly in 96 of 21616patients retrospectively, and prenatal bowel perfo-ration and/or meconium peritonitis in 11 of these.Prenatal findings of patients, having the diagnosisof postnatal meconium peritonitis or pseudocyst,were intraabdominal cystic echogenic structuresaccompanied by dilated bowel loops (4 cases),dilated bowel loops (3 cases), free intraabdominalfluid (2 cases), echogenic bowel without dilation(1 case).7

The diagnosis of fetal gastrointestinal systemanomalies by MR is supplied by abnormal bowelloop dimensions, abnormal bowel loop signal and


abnormal intraabdominal structures accompaniedby normal bowel imaging findings. The normalimaging findings of bowel loops, the presence ofintestinal dilation and location, and imaging ofpostatretic bowel loop seem to be reliable in therecognition of meconium ileus and peritonitis byMR.2 But as in our case, it cannot also be recog-nized by prenatal obstetric ultrasonography andMR imaging.

MR seems to be more informative for the diag-nosis of severe malformations such as megacysti-tis-microcolon-intestinal hypoperistalsis syndrome,multiple atresia, congenital short bowel.2

Meconium ileus and peritonitis should be consid-ered in the differential diagnosis, when a mass inthe fetal abdomen, accompanied by findings espe-cially ascites, intraabdominal calcification, boweldilation is seen at ultrasonography and MR imag-ing. More experience is needed for this subject andthe indications of MR imaging should be deter-mined.

References

1. Anteby EY, Yagel S. Route of delivery of fetuses with struc-tural anomalies. Eur J Obstet Gynecol Reprod Biol 2003;106:5-9.

2. Veyrac C, Couture A, Saguintaah M, Baud C. MRI of fetal GItract abnormalities. Abdom Imaging 2004; 29: 411-20.

3. Courteville JE, Gray DL, Langer JC. Bowel abnormalities inthe fetus-correlation of prenatal ultrasonographic findingswith outcome. Am J Obstet Gynecol 1996; 175: 724-9.

4. Saguintaah M, Couture A, Veyrac C, Baud C. MRI of thefetal gastrointestinal tract. Pediatr Radiol 2002; 32: 395-404.

5. Elchalal U, Ben-Shachar I, Nadjari M, Gross E, Appleman Z,Caspi B. Prenatal diagnosis of acute bladder distention as-sociated with sacrococcygeal teratoma-a case report.Prenatal Diagnosis 1995; 15: 1160-4.

6. Hertzberg BS, Kliewer MA, Bowie JD. Sonography of the

fetal gastrointestinal system. In: Sonography in Obstetrics

and Gynecology: Principles and Practice. Fleischer AC,

Manning FA, Jeanty P, Romero R (Eds). Fifth Edition, Pren-

tice-Hall International Inc, Appleton and Lange, Conneticut,

1996. 411-431.

7. Eckoldt F, Heling KS, Woderich R, Kraft S, Bollmann R,

Mau H: Meconium peritonitis and pseudo-cyst formation:

prenatal diagnosis and post-natal course. Prenat Diagn

2003; 23: 904-8.

8. Shyu MK, Shih JC, Lee CN, et al. Correlation of prenatal ult-

rasound and postnatal outcome in meconium peritonitis.

Fetal Diagn Ther 2003; 18: 255-61.

9. Budorick NE. The fetal musculoskeletal system. In: Ult-

rasonography in Obstetrics and Gynecology. Callen PW

(Ed). Forth edition. WB Saunders Company, Philadelphia,

Pennisylvannia, 2000. 366-369.

10. Neural tube defects. In: Diagnostic Imaging of Fetal

Anomalies. Nyberg DA, McGahan JP, Pretorius PH, Pilu G

(Eds). Lippincott Williams@Wilkins, Philadelphia, Pennisyl-

vannia, 2003. 324-329.

11. Siegel MJ, Pediatric and adolescent pelvis. In: Computed

Tomography and Magnetic Resonance imaging of the

whole body. Haaga JR, Lanzieri CF, Gilkeson RC (Eds).

Forth edition. Mosby, St Louis, Missouri, 2003. 2090-2091.

12. Chisholm CA, Heider AL, Kuller JA, Von Allmen D,

McMahon MJ, Chesneir NC. Prenatal diagnosis and perina-

tal management of fetal sacrococcygeal teratoma. Am J

Perinatol 1999; 16: 47-50.

13. Kamata S, Nose K, Ishikawa S, et al. Meconium peritonitis

in utero. Pediatr Surg Int 2000; 16: 377-9.

14. Chalibinski K, Deutinger J, Bemaschek G. Meconium peri-

tonitis: extrusion of meconium and different zoographical

appearances in relation to the stage of disease. Prenat

Diagn 1992; 12: 631-6.



Abstract

Background: Patau syndrome has been estimated to occur in 1 in 12.000-29.000 live births, and the risk is increased withadvanced maternal age advanced maternal age.

Case: The ultrasonography was applied to a 40 years old mother and flat nose, holoprosencephaly, cleft palate and cleft lipwere seen. Holoprosencephaly, multicystic kidney, cleft palate and cleft lip were found in the autopsy examination of the fetus.

Keywords: Holoprosencephaly, cleft palate, cleft lip multicystic kidney, trisomy 13, prenatal diagnosis.

Patau sendromu (trizomi 13): otopsi olgusu

Amaç: Patau sendromu 12.000-29.000 canl› do¤umda bir görülmektedir ve ileri anne yafl› ile risk artmaktad›r.

Olgu: 40 yafl›ndaki annenin yap›lan ultrasonografisinde, hipotelorizm, bas›k burun, holoprozensefali, yar›k damak ve yar›k dudaktespit edildi. Fetusun otopsi incelemesinde holoprozensefali, multikistik böbrek, yar›k damak ve yar›k dudak saptanm›flt›r.

Anahtar Sözcükler: Holoprozensefali, yar›k damak, yar›k dudak, multikistik böbrek, trizomi 13, prenatal tan›.

Patau Syndrome (Trisomy 13):Autopsy Case

Nihal K›l›nç1, Bülent Demir2, Diclehan Orhan3, Murat Yayla2

1Department of Pathology, Faculty of Medicine, Dicle University, Diyarbak›r2Department of Gynecology and Obstetrics, Faculty of Medicine, Dicle University, Diyarbak›r

3Department of Genetics, Faculty of Medicine, Dicle University, Diyarbak›r

Correspondence: Dr. Nihal K›l›nç, Dicle Üniversitesi T›p Fakültesi, Patoloji Anabilim Dal› 21280 Diyarbak›r, e-mail: [email protected]

Background

Cytogenetics of Patau syndrome is described by

Patau et al and clinical phenotype is described by

Smith.1,2 In most of cases, there is nondysjunction-

one of morphological chromosomal anomalies.

There is approximately 20% translocation and less

than 10% mosaicism in cases.3 Patau syndrome oc-

curs in about 1 out of every 12.000-29.000 live

births and the risk is increased with advanced ma-

ternal age.4 Chromosome 13 is larger than chromo-

some 21 and therefore anomalies are multiple and

more severe in trisomy 13. Midline anomalies, fa-

cial defects, holoprosencephaly, cardiac defects

omphalocele, polycystic kidney disease and poli-

dactyly are prominent in sonography.5

Children with Patau Syndrome die in a short

time after birth. Seldomly children survive into

their first year.6 Patau Syndrome is presented as a

case report because it is seen rarely and the first

experience of our clinic.

Case

40-year-old mother with G4, P3, L3, A1, first

degree of relationship with her husband and no

any prenatal follow up hypotelorism, holoprosen-

cephaly (Figure 1), flat nose, cleft lip, cleft palate

determined in ultrasonography applied at 24 ges-

tational week. Pregnancy terminated with permis-

sion of the family. The birth was via normal vagi-

nal delivery with 1/0 apgar score. In autopsy

examination, fetus was 1650 g in weight, 35 cm in

length and headcircumference was 20 cm with

cleft palate and cleft lip. Plasenta was 350 g in

weight with normal appearance (Figure 2).

Thoracal and abdominal organs located in their

normal anatomic positions. Superior longitudinal

fissure was not seen in cranial dissection. Bilateral

kidney dimensions were 4x2x1.2 cm. Microscopi-

cally holoprosencephaly and bilateral polycystic

kidneys determined (Figure 3). Karyotype made by

GTG band technique after amniosynthesis was 47,

XX+13.

DiscussionClinical signs of Patau syndrome (trisomy 13)

firstly described at 1967 by Bartolin.7 Patau et al.described syndrome caused by an extra copy ofchromosome 13 in group D. Patau syndromeoccurs in about 1 out of every 12.000-29.000 livebirths but 100 times more in spontaneous abor-tus.4.7

Major signs of trisomy 13 are motor and mentalretardation, microcephaly, microphthalmia, holo-prosencephaly, hypotelorism, cleft palate, cleft lip,cardiovascular, genitourinary, ocular malforma-tions and early death.8

Chromosomal analysis is necessary for defini-tive diagnosis. Chromosome 13 is larger than chro-mosome 21 and therefore anomalies are multipleand more severe in trisomy 13.9

Generally Patau syndrome is caused by classi-cal trisomy 47, XX+13 (80%) and also but less fre-quently (10%) translocation, structural changes andother chromosomal disorders like (5%) mos-saicism.7,9 In this case some characteristical signs ofPatau syndrome was determined in ultrasonogra-phy applied in perinatology clinic in routine con-trol. In karyotype analysis classical type 47, XX+13was determined.

Magenis et al announced that 28% of patientswith Patau syndrome die in their first week, 44% intheir first month and 86% in their first year. Taylorannounced the mean life expectancy 89.2+ 29.9days, but Redheedran et al12 and Zoll et al.7

announced that some children with trisomy 13 sur-vive into their teens. Our case died one day afterbirth. Patients with Patau syndrome are trisomic forchromosome 13, and there is 3 chromosomeinstead of 2. With extra chromosome in group D,in karyotype there is 47 XX+D total chromosome.

K›l›nç N et al., Patau Syndrome (Trisomy 13): Autopsy Case170

Figure 1. Ultrasonographic appearance of holoprosen-cephaly.

Figure 2. Macroscopic appearance of flat nose, cleft palateand cleft lip malformations.


Figure 3. Cystic tubular structures with different dimensions.

20% of cases have 46 chromosome but they have

Robertsonian type of translocation between chro-

mosome 13 and 14.13

Golstein et al14 established that mother age is

over 35 in their study. Mother age is advanced in

cases of chromosomal nondisjunction. Mean moth-

er age is 39 in this group. In our case mother age

was 40. In translocation and mosaicism type of tri-

somic cases, mother or father may be carrier and

other children have risk of disease. If mother and

father are not carriers, recurrence risk is less than

1%.

Boyd et al15 reported that mothers who have

fetus with trisomy 13 are at risk of preeclampsia

more than mothers who have fetus with trisomy 21

and 18 or with no chromosomal anomaly.

As a result, trisomy 13 is known as one of the

oldest chromosomal disorder. Autosomal cytoge-

netic abnormalities should be considered in case

of mothers with preeclampsia, mothers older than

35 years old and who have spontaneous abortus

and genetic consulting should be recommended.

Pregnant woman can be followed up in perinatol-ogy clinics for early diagnosis of fetus with abnor-mality.

References

1. Patau K, Simith DW, Therman E, Inhorn SL, Wagner HP.Multiple congenital anomalies caused by an extra autoso-me. Lancet 1960; 1:790-3.

2. Smith DW. Recognizable patterns of human malfarmations.2nd ed. Philadelphia: WB Saunders, 1982.

3. Zellweger H, Simpson J. Chromosomes of man. Philadelp-hia: JB Lippincott, 1997.

4. Nielsen E, Sillesen J. Incidence of chromosome aberrati-ons arising in 11, 148 newborn children. Hum Genet 1975;30: 1.

5. Öndero¤lu LS. Dismorfik sendromlar›n tan›s›nda ultrasonog-rafi. Obstetrik ve Jinekolojik Sürekli E¤itim Dergisi 1997; 145-6.

6. Yenerman M. Genel Patoloji. ‹stanbul,Tayf, 1994 ;423-4.

7. Zoll B, Wolf J, Lensing-Hebben D, Pruggmayer M, ThorpeB. Trisomy 13 (Patau syndrome) with an11-year survival.Clin Genet 1993; 43: 46-50.

8. Rios A, Furdon SA, Adams D, Clark DA. Recognizing theclinical features of Trisomy 13 syndrome. Adv NeonatalCare 2004; 4: 332-43.

9. de Grouchy, Turleau C. Autosomal Disorders. Principles andPractice of Medical Genetics. New york, 2nd, 1990; 256-8.

10. Magenis ER, Hecht F,Milham S. Trisomy 13 (D9 syn-drome:studies on parental age, sex ratio, and survival. JPediatr 1968; 73: 222-8.

11. Taylor AJ. Autosomal trisomy 13 (Patau’s syndrome): a

detailed 27 cases of Edward’s syndrome and 27 cases of

Patau’s syndrome. J Med Genet 1968; 5: 227-52.

12. Redheendran R, Neu RL, Bannerman RM. Long survival in

trisomy-13-syndrome: 21 cases including prolonged sur-

vival in two patients 11 and 19 years old. Am J Med Genet

1981; 8: 167-72.

13. Tunca Y, Kadandale JS, Pivnick EK. Long-term survival in

Patau syndrome. Clin Dysmorphol 2001; 10: 149-50.

14. Goldstein H, Nielsen KG. Rates and survival of individuals

with trisomy 13 and 18. Data from a 10-year period in Den-

mark. Clin Genet 1988; 34: 366-72.

15. Boyd PA, Lindenbaum RH, Redman C. Pre-eclampsia and

trisomy 13: a possible association. Lancet 1987; 22: 425-7.

K›l›nç N et al., Patau Syndrome (Trisomy 13): Autopsy Case172


Abstract

Backround: Pregnancy is a physiologic state with a markedly increased risk for venous thromboembolism. Deep vein thrombo-sis (DVT) is estimated to affect 0.71 in every 1000 pregnancies.

Case: A pregnant women at 36 week of gestation was hospitalized due to left leg pain and edema which was determinatedDVT in the venous doppler ultrasonography and the case was performed the cesarean section for fetal distress, immediately.Respiratory distress and hypoxemia was started in the postanaesthetic care unit. Pulmonary embousi was determineted in thethorax computed tomography.

Conclusion: Cooperation of obstetrican and anaesthetist require during evaluation of pregnant which had risc factors for venousthromboembolism. So early diagnose and management of pulmonary embolus can be started with carefully observation, whichmay be reduce mortality and morbidity, in the postanaesthetic care unit.

Keywords: Venous thromboembolism, pulmonary embolism, pregnancy.

Gebelikte tromboembolik olaylar ve sezaryen sonras› pulmoner Emboli: olgu sunumu

Amaç: Gebelik venöz tromboembolizm için risk faktörlerinin yo¤un olarak artt›¤› bir süreçtir. Derin ven trombozu (DVT) her100.000 gebenin 71’inde saptanabilmektedir.

Olgu: 36 haftal›k gebe olgu, sol bacak a¤r›s› ve flifllik flikayeti ile kad›n do¤um klini¤ine kabul edildi. Venöz Doppler ultrasonog-rafide sol bacak da derin ven trombozu izlenen olgu, fetal distress nedeniyle acil olarak sezaryen operasyonuna al›nd›. Anesteziderlenme ünitesinde hipoksi ve solunum s›k›nt›s› geliflen olguda toraksa yönelik bilgisayarl› tomografide pulmoner emboli sap-tand›.

Sonuç: Venöz tromboembolizm için risk faktörlerine sahip gebeler de¤erlendirilirken anestezist ve obstetrisyenlerin ifl birli¤i ge-rekir. Dikkatli gözlem ile pulmoner embolinin erken teflhis ve tedavisine anestezi derlenme ünitesinde bafllanabilir ve bu mortali-te ve morbiditeyi azaltabilir.

Anahtar Sözcükler: Venöz tromboembolizm, pulmoner emboli, gebelik.

Thromboembolic Cases in the Pregnancy andPulnomery Embolism after Cesarean:

Case Presentation

Nimet fieno¤lu1, Hafize Öksüz1, Beyaz›t Zencirci1, Meral Ezberci1, K›ran Gürkan2, Okur Nazan3

1Department of Anaesthesielogy and Reanimation,2Department of Obstetrics and Gynecology , 3Department of Radiodiagnostics,

Hospital of Medical Faculty, Kahramanmarafl Sütçü ‹mam University, Kahramanmarafl

Correspondence: Dr. Nimet fieno¤lu, Kahramanmarafl Sütçü ‹mam Üniversitesi T›p Fakültesi Hastanesi, Anesteziyoloji ve ReanimasyonAnabilim Dal›, Kahramanmarafl, e-mail: [email protected]

Background Pregnancy is a physiologic process with

markedly increased thromboembolic complica-

tions. Venous thromboembolism is an uncommon

illness causing maternal mortality and morbidity.1.2.3

It is mentioned that in the periods of perinatal,

peripartum and postpartum, especially when per-forming the birth as cesarean, this risk isincreased.4 In the presented case, there were deepvein thrombosis (DVT) and hematological illnessin the personal history and there was respiratorydistress in the postanaesthetic care unit.Obstetricians and anesthesia and intensive caredoctors must absolutely take into considerationthat the risk of pulmonary embolism increaseshigher in the cesarean cases with postoperativehypoxemia and respiratory distress developmentthan the other cases.

Case Female case at the age of 22, having 36-37

weeks of pregnancy applied to our hospital withthe complaints of left leg pain and distention.There were edema in the left leg and heat increaseand peripheral pulses were detected. In her per-sonal history, she was diagnosed thalassemia inter-media in her pregnancy three years ago and afterthe caesarean surgery she had also splenectomyoperation. DVT was detected in the case that leftleg Doppler ultrasonography was taken urgently,cure was started by enoxaparin sodium 6000 IU astwo dosages per day subcutaneous. In the secondday, fetal distress was detected and she was

urgently taken for cesarean operation. Thiopental8 mg/kg-1, lidokalin 1.5 mg/kg-1 and rocuronium0.6 mg/kg-1 and anesthesia induction and orotra-cheal intubation was performed to the patient towhom premedication was not implemented. In the5th minute following the induction, a 2300 grammale baby was born whose APGAR score was 6 inthe fist minute and 8 in the fifth minute.Anesthesia continuation was provided with 50%oxygen and 0% nitrogen protoxic and followingcord clamping 1 mcg.kg-1 fentanyl as intra venousand sevofluran in a concentration of 0.8 minimalalveolar. Patient having no peroperative anesthet-ic problem was awakened after the operation last-ing 40 minutes. The patient was taken to postop-erative caring unit, oxygen saturation 90-92%, res-piration number 24 minutes-1, blood pressure20/85 mmHg and heart rate 120 pulse/min-1 wasdetected even the patient was supported by 5L/min-1 oxygen with nasal cannula. Case, whosepH 7.425, pCO2 30.8 mmHg, PO2 55 mmHg, HCO320.3 mmol/L, BEb-3.2 mmol/L, spO2 89.4% wasdetected in blood gas was taken for monitoring inthe anesthesia intensive care unit. In the preoper-ative blood count, hemoglobin was 11.3 g/dL,hematocrit was 33.7%, leukocyte was 27.000 K/UL,platelet, was 504, k/UL, in the blood biochemistry,total bilirubin was 1.09 mg/dL, conjugate bilirubin

fieno¤lu N et al., Thromboembolic Cases in the Pregnancy and Pulnomery Embolism after Cesarean: Case Presentation174

Figure 1. View of the lungs in the case.


was 0.37 mg/dl, lactic dehydrogenase was 934 U/Land the other parameters were in the normal bor-der. Respiratory sounds by listening lowered in thebasal and uncommon rals exist. There was no sig-nificant pathological look in the lung diagram.Suspecting from PE because of the clinical find-ings, lung diagram was taken and contrast spirallung tomography was taken. There was no abnor-mal condition in the lung diagram (Figure 1). Inthe dynamic intravenous contrasted computerizedtomography for thoracic investigation (by Appling120 ml nonionic contrasted substance at a speed of3 ml/second) in the mediastinal window, in theright main pulmonary artery having a diameter of1 cm, thrombus adopted multiple hipodens areaswere detected (Figure 2). In the paranchymal viewof the tomography, in the right hemithorace, in thebronchovascular marks, embolism secondary rela-tive decrease was detected when compared withthe symmetric (Figure 3). PE was diagnosed for the

case with the radiological and clinical findings andthe enoxaparin sodium treatment was changedwith intravenous heparin treatment (30.000 U/daydosages). The case, which was supported by oxy-gen 8 L/minute, sufficient peripheral oxygen satu-ration, was reached. Thrombotic findings degradedwith the heparin treatment and oral warfarin treat-ment was stated in the ninth day (7.5 mg/day). Thecase was passed to cardiac surgery in the 10th dayfor the follow and treatment of deep vein throm-bosis, and was discharged in good health.

DiscussionThe postanaesthetic care period, there can be

respiration failures and reasons of hypoxia, pneu-mothorax, pulmonary edema, pulmonary aspira-tion, and secretion, obstruction with blood andclot and bronchospasm.5 Pulmonary emboli (PE)should also be considered for the patients in therisk group as another reason.

Figure 2. Thrombus in the contrasted computerized tomography (arrow).

As to the woman in the same age group, it isstated that the thromboembolism incidents increas-es by 5 times in the pregnancy.1 Physiological andanatomical changes in the pregnancy are as adecrease venous turning as a result of venousrepletion and volume increase. Hypercoagulability,stasis and endothelial injury are the three factorsfor the venous thromboembolism and these can beseen in the physiological process of the pregnan-cy.6 The reasons for them are hormonal as a resultof progesterone and estrogen increase and theyare more obvious in the progressive trimester.1

Another reason is that the growing uterus mechan-ically obstructs the pelvic veins. Coagulation fac-tors increase in the pregnancy, coagulationinhibitors decrease and fibrinolotic capacitydecrease and this causes hypercoagulability.7 It isalso stated that the thrombocyte activity rises in thepregnancy. Birth, however, because of the pressby the surgery or surgery devices, causes vascularinjury and changes in the uteroplasental surface.The risk of venous thromboembolism can increase

in the cases of preterm birth, preeclampsia, hem-orrhage, sepsis, birth with intervention of cesareanand multiparity.1 It is thought that the risk factorincreases especially in the third trimester and post-partum period. The risk of venous thromboem-bolism increase by 5-10 times in the pregnancy.This risk reaches it maximum level especially afterthe delivery.8

It is informed that the risk factor about DVT inthe pregnancy is less than 35 age, long time bedrest and inactivity, pelvis or leg trauma and obesi-ty. Additional risk factors are cesarean birth, hem-orrhage, multi-parity, varicose veins, previousthromboembolic incidences, hereditary oracquired thrombophilia and preeclampsia.9,10,11

DVT affects 71 of every one hundred thousandpregnant.12

The case having thromboembolic illness in thehistory, hematological illness as thalassemia inter-media is the additional risk factors for deep veinthromboses. By adding the factors such as preg-nancy and birth with cesarean, the risk of PE


Figure 3. Decrease in the bronchovascular view in the right hemithorax.

increased for the case. It must be very careful inthe peripartum period and especially intrapartumand postpartum periods. It is stated that DVTincreases in the left leg in the pregnancy.12 The factthat the DVT developed in the left leg in the casesupports that information.

Although it develops uncommonly, PE hasimportance because of maternal mortality andmorbidity. PE incidence is stated 1/1000-2000 forsome and 1/2500-10.0001-12 for others. Source ofthe emboli is known as proximal veins in the legor pelvis or calf veins by many researchers.13 Themost important factor in its etiology is the move ofthrombus in the active peripheric veins. Detectionof the PE can be difficult because of the variousfindings. Thorax diagram, electrocardiogram(ECG), sensitivity of the blood gas tests and speci-fication are not enough in the routine laboratorystudies. Most commonly reported findings of thePE are dyspnea, tachypnea and pleural based chestpain. Findings and symptoms such as anxiety,cough, and ral in the lungs are found approxi-mately in the half of the patients.1 ECG, thorax dia-gram, analysis of blood gas supports the diagnosisand helps to separate from other reasons in the eti-ology. Ventilation/perfusion scintigraphy is alsosuggested to support the diagnosis. Some non-spe-cific abnormalities such as increase in hemidi-aphragm, consolidation, unilateral pleural effu-sions, atelectasis can be seen in the PE patients.Decrease of the arterial oxygen pressure can beseen in the case of PE but it is not specific.

Dyspnea and tachypnea and hypoxia are seenin our case in the postoperative collection unit.Findings of hypocapnia and hypoxia were the sup-portive blood gas findings for pulmonary emboli.For the reason that the monitoring the lung dia-gram did not support the finding, contrast spirallung tomography was taken and PE pre-diagnosiswas supported. Some conditions such as pneumo-nia, atelectasia causing hypoxia must be thought inthe distinctive diagnosis. These possibilities can beexcluded by lung diagrams and spiral thorax CT.Finding of deep vein thrombus may not beremarkable every time and the diagnosis of PE canbe difficult. But the early detection is important, itmust be diagnosed without delay and treatmentmust be started.15

If PE diagnosis is late of is not made, it cancause maternal morality. Diagnosis of PE and DVTfor the pregnant requires objective view such asfor the patients who are not pregnant. Reliability oflaboratory tests such as D-limer is restricted. Itmust be supported by clinical and radiologicalfindings first of all.

As a conclusion; conditions such as pregnancyand cesarean operation are risk factors for DVTand PE. It is obvious that special attention must bepaid for the patient with the risk group. Distinctivediagnosis of pulmonary emboli and its treatmentmust be made for the cases that hypoxemia devel-ops in the postoperative care unit after cesareanoperation considering all these risks.

References

1. Toglia MR, Nolan TE. Venous Thromboembolism DuringPregnancy: A Current Review of Diagnosis and Manage-ment. Obstetrical Gynecological Survey 1997; 52: 60-72.

2. Pabinger I, Grafenhofer H.Thrombosis during pregnancy:risk factors, diagnosis and treatment. Pathophysiol HaemostThromb 2002; 32: 322-4.

3. Rochat RW, Koonin LM, Atrash HK, et al. Maternal mortalityin the United States: Report from the Maternal Mortality Col-laborative. Obstet Gynecol 1988; 72: 91-7.

4. Gherman RB, Goodwin TM, Leung B, Byrne JD, MontoroM. Incidence, clinical characteristics, and timing of objec-tively diagnosed venous thromboembolism during preg-nancy. Prim. Care Update Ob Gyns 1998; 5: 155-6.

5. Morgan GE, Michail MS, Murray MJ. Clinical Anest-hesiology. 3th ed. McGraw-Hill. 2002; 945-6.

6. Phillips OP.Venous thromboembolism in the pregnantwoman. J Reprod Med 2003; 48(Suppl): 921-9.

7. Gerbasi FR, Bottoms S, Farag A et al. Increased intravas-cular coagulation associated with pregnancy. ObstetGynecol 1990; 75: 385-9.

8. Jacobsen AF, Drolsum A, Klow NE, Dahl GF, Qvigstad E,Sandset PM. Deep vein thrombosis after elective cesareansection. Thromb Res 2004; 113: 283-8.

9. Greer IA. Prevention of venous thromboembolism in preg-nancy. Eur J Med Res 2004; 30: 135-45.

10. Colman-Brochu, Stephanie MSN, RN, Deep Vein Throm-bosis in Pregnancy. MCN, American Journal of MaternalChild Nursing 2004; 29: 186-92.

11. Bates SM, Ginsberg JS. Thrombosis in pregnancy. CurrOpin Hematol 1997; 4: 335-43.

12. Ray JG, Chan WS. Deep Vein Thrombosis During Preg-nancy and the Puerperium: A Meta-Analysis of the Periodof Risk and the Leg of Presentation. ObstetricalGynecological Survey 1999; 54: 265-71.


13. Franks AL, Atrash HK, Lawson HW, et al. Obstetrical pul-

monary embolism mortality, United States, 1970-1985. Am J

Public Health 1990; 80: 720-2.

14. Dixon JE. Pregnancies complicated by previous throm-

boembolic disease. Br J Hosp Med 1987; 37: 449-52.

15. Stone SE, Morris TA. Pulmonary embolism and pregnancy.

Crit Care Clin 2004; 20: 661-77.

16. Chan WS, Ginsberg JS. Diagnosis of deep vein thrombosis

and pulmonary embolism in pregnancy. Thromb Res 2002;

15: 85-91.



Abstract

Background: The review of diagnostic and therapeutic requirements of a noncommunicating uterine horn pregnancy case asa rare situation according to the existing literature.

Case: A 26 years old, G4 P3 L2 A0 D&C 0 pregnant woman introduced to emergency unit of our hospital with serious abdom-inal pain and fainting. Arterial blood pressure of the patient was 90/40 mmHg and her heart beat count was 110 beats perminute at admission. Intraoperatively, a dead fetus at 17 weeks of gestation has been seen in the abdominal cavity as a resultof non-communicating uterine horn rupture.

Conclusion: Rudimentary horn pregnancy is a rare pregnancy presentation that can not always be diagnosed sonographicallyand excision of the rudimentary horn is the advised management.

Keywords: Rudimentary, rupture, uterine anomaly, diagnostic difficulty, management.

Onyedi haftal›k nonkomunike redimenter uterin horn gebeli¤i ve uterin rüptür: olgu sunumu

Amaç: Nadir bir durum olan nonkomunike rudimenter uterin horn gebeli¤inin ruptürü ile karfl›lafl›ld›¤›nda tan› ve tedavide ya-p›lmas› gerekenlerin varolan literatüre göre bir olgu sunumu ile de¤erlendirilmesi.

Olgu: Yirmi alt› yafl›nda, G4 P3 Y2 A0 D&C0 olan gebe hastanemiz acil servisine fliddetli kar›n a¤r›s› ve bayg›nl›k flikayeti ile bafl-vurdu. Arterial kan bas›nc› 90/40 mmHg, nab›z 110 at›m/dakika olarak tespit edildi. Transvajinal ultrasonografide bir taraf› rup-türe olmufl çift uterus görünümü görüldü. ‹ntraoperatif de¤erlendirmede nonkomunike rudimenter horna yerleflim gösteren 17haftal›k fetüsün, uterin rüptür sonucu bat›na ç›kt›¤› görüldü.

Sonuç: Rudimenter horn gebeli¤i tan›s› ultrasonografi ile her zaman konulamayan, maternal ve perinatal mortalite riski yüksekolan nadir bir gebelik fleklidir. ‹lerleyen gestasyonel hafta ile beraber uterin rüptür riski önemli oranda artmaktad›r.Tan›s› konul-du¤unda eksize edilerek ç›kart›lmas› uygun yaklafl›m olarak kabul edilmektedir.

Anahtar Sözcükler: Rudimenter, ruptür, uterin anomali, tan›sal zorluk, yönetim.

17 Week Non-Communicating RudimenterUterine Horn Pregnancy and Uterine Rupture:

Case Report


Department of Perinatology, Zekai Tahir Burak Training and Research Hospital, Ankara

Correspondence: Dr. Serkan Kahyao¤lu, Zekai Tahir Burak Kad›n Hastal›klar› ve Do¤um Hastanesi, Perinatoloji, Ankarae-mail: [email protected]

BackgroundOverall incidence of congenital Mullerian duct

anomalies is 0.1-3.8% in women. Unicorniateuterus is the least frequent Mullerian anomaly andseen 4.4%.1 It is assumed that there is a migration

defect to proper location of one of Mullerianducts.2 American Society for ReproductiveMedicine (ASRM) divided unicorniate uterus into 4groups; communicating rudimentary horn unicor-niate uterus, noncommunicating rudimentary horn

Kahyao¤lu S et al., 17 Week Non-Communicating Rudimenter Uterine Horn Pregnancy and Uterine Rupture: Case Report180

Figure 1. Sonographic appearance of fetus and plasenta located in abdominal cavity justnear to uterus.

unicorniate uterus, isolated unicorniate uterus andnoncommunicating rudimentary horn unicorniateuterus with no cavity.3 Unicorniate uterus may ca-use spontaneous abortus, ectopic pregnancy, ab-normal presentation, intrauterine growth restrictionand preterm labour. Implantation in rudimentaryhorn is related with high rate of pregnancy lossand tubal pregnancy. Most of them are noncom-municating and do not contain functional endo-metrium therefore asemptomatic. 40% of patientshave urinary system anomalies. Myometrium in ru-dimentary horn is thin. Therefore, the risk of uteri-ne rupture is high in pregnancies in that location.4

Due to potential problems prophylactic excision isrecommended when it is met.5

Case26-year-old G4, P3, L2, A0, D&C0 pregnant wo-

man introduced to emergency unit of our hospitalwith severe abdominal pain and fainting. In res-pect of her history, she had irregular menstrualcycle and was 13 week pregnant according to herlast menstrual period. Left lower quadrant painand tenderness in servical movements determinedin pelvic examination. Uterine enormity was notevaluated due to voluntary defence. Arterial blood

pressure was 90/40 mmHg and heart rate was 110beats per minute. Free fluid and an extrauterinedead fetus at 17 week 5 day of gestation has beenseen in right upper quadrant by abdominal sonog-raphy. Transvaginal sonography revealed bicornu-ate uterus (Figure 1). Preoperatively ruptured hornwith echogenic plasenta and echolugent myomet-rium around plasenta revelaed by sonography butdid not differentiated from abdominal pregnancy(Figure 2). Hemoglobin level was 8.1 g/dl beforeoperation and she was admitted to laparatomy. Int-raoperatively a dead fetus at 17 weeks of gestationhas been seen in the abdominal cavity as a resultof noncommunicating uterine horn rupture (Figure3). Fetus has taken and 1500 cc hemorrhagic fluiddrained from abdominal space. Rudimentary hornhas excisied with its point connected to uterus.Then uterus sutured with baseball technique (Figu-re 4). 2 units of blood transfused to patient andthere was no any complication in postoperativefollow up.

DiscussionRudimentary horn pregnancy is a rare pregnan-

cy presentation with high maternal and perinatalmortality risk and cannot always be diagnosedsonographically. There are a few term pregnancies


Figure 2. Ruptured rudimentary uterine horn with echolucent myometrium layeraround echogenic placenta just near to fetal head in abdomen

Figure 3. Intraoperative digital photograph of fetus and placenta that rupture rudimentary horn and go toabdomen.

in rudimentary horn in the literature and they havehigh maternal and perinatal mortality rates. Incommunicating rudimentary horn cases mecha-nism of pregnancy is clear but in noncommunicat-ing type, transperitoneal migration of sperms isassumed. In both conditions there is a thinmyometrial layer and noncomplete uterine cavitydevelopment.6 The risk of uterine rupture increas-es with advanced gestational age. It is a rare con-dition but due to clinical outcome and effect onfertility of patient it causes important gynecologicaland obstetric problems.7 Acute abdomen, dysmen-orrhea, dyspareunia or chronic pelvic pain may beclinical outcome, when there is hemometria,pyometria, torsion, endometriomas with retrogrademenstruation in rudimentary horn. Rupture in non-communicating rudimentary uterine horn pregnan-cy is a frequent outcome. A concomitant hetero-topic pregnancy should be considered with rudi-mentary horn intrauterine pregnancy.8 Thereforeexcision assumed a proper approach when preg-nancy diagnosed.

References

1. Speroff L, Glass RH, Kase NG. Clinical Gynecologic Endoc-rinology and Infertility. Sixth Edition, 1999. ISBN 0-683-30379-1.

2. Panayotidis C, Abdel-Fattah M, Leggott M. Rupture of rudi-mentary uterine horn of a unicornuate uterus at 15 weeks'gestation. J Obstet Gynaecol 2004; 24(3): 323-4.

3. The American Fertility Society. The American FertilitySociety classifications of adnexal adhesion, distal tubal occ-lusion, secondary to tubal ligation, tubal pregnancies, Mul-lerian anomalies and intrauterine adhesion. Fertil Steril1988; 49: 944-55.

4. Daskalaskis G, Pilalis A. Rupture of noncommunicationRudimentary Uterine Horn Pregnancy. Obstet Gynecol 2002;100: 1108-10.

5. Sefrioui O, Azyez M, Babahabib A, Kaanane F, Matar N.Pregnancy in rudimentary uterine horn: diagnostic and ther-apeutic difficulties. Gynecol Obstet Fertil 2004; 32(4): 308-10.

6. Kuflçu NK, Laçin S, Kartal Ö. Rupture of rudimentary hornpregnancy at the 15 th week of gestation: a case report. EurJ Obstet Gynecol Reprod Biol 2002; 102: 209-10.

7. Atmaca R, Germen AT, Burak F, Kafkasl› A. RudimenterHornlu Unikornuat Bir Olguda Akut Bat›n. Artemis 2003;Vol 4(4): 74-6.

8. Ozan H, Kimya Y, Esmer A, Karahasan M. A Case ofHeterotopic Pregnancy. Gynecology Obstetrics and Rep-roductive Medicine 2001; Vol 7 (2): 172-3.

Kahyao¤lu S et al., 17 Week Non-Communicating Rudimenter Uterine Horn Pregnancy and Uterine Rupture: Case Report182

Figure 4. Apperance of uterus after intraoperative excision of rudimentary uterine horn

Volume 13 / Issue 3 / 2005

PERINATALJOURNAL

Contents

129

138

142

148

152

158

163

169

179

173

Role of Doctors, Midwives and Nurses in Oxytocin AdministrationNurdan Demirci, Özlem Gürkan, Hediye Arslan, Zübeyde Ekfli

Frequency of Genetic Thrombophilia in Severe Intrauterine Growth RestrictionRag›p Atakan Al, Serdar Yalvaç, Esmen Öztürko¤lu, Erol Akkök, Ömer Kandemir, ‹smail Dölen

Maternal Serum Concentrations of Metabolites of Nitric Oxide in PreeclampsiaLevent Tütüncü, Emine Özdemir, Ercüment Müngen, Ali Rüfltü Ergür, Yusuf Z. Yergök

Conservative Managemenet of Twin Pregnancy After Delivery of One Fetus at theSecond Trimester of the Pregnancy


Relationship of Early Diastolic Notch in Uterine Artery Doppler Measurements WithPregnancy Complications in Low Risk Pregnancies

Faik Gürkan Yaz›c›, Ekrem Tok, S›tk› Gülhan, Devrim Ertunç, Gülay Özdemir, Saffet Dilek

Retrospective Analysis of Polyhydramnios CasesAhmet Kale, Nurten Akdeniz, Mahmut Erdemo¤lu, Ahmet Yal›nkaya, Murat Yayla

A Case Report of Meconium Ileus-Peritonitis with a Prenatal Diagnosis ofSacro-Coccygeal Teratoma

Baflak Baksu, ‹nci Davas, Jale Özgül, Figen Ezen, Alper Özel, Gülden Yenice, Mehmet Yalç›n

Patau Syndrome (Trisomy 13): Autopsy CaseNihal K›l›nç, Bülent Demir, Diclehan Orhan, Murat Yayla

Thromboembolic Cases in the Pregnancy and PulnomeryEmbolism after Cesarean: Case Presentation

Nimet fieno¤lu, Hafize Öksüz, Beyaz›t Zencirci, Meral Ezberci, K›ran Gürkan, Okur Nazan

17 Week Non-Communicating Rudimenter Uterine Horn Pregnancy and UterineRupture: Case Report


Research Articles

Case Reports

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