ISSN 1305–3124 PERINATAL

The Official Publication of

Perinatal Medicine Foundation

Turkish Perinatology Society

Turkish Society of Ultrasound in Obstetrics and Gynecology

ISSN 1305–3124

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PERINATALJOURNAL

20 YEARS

w w w . p e r i n a t a l j o u r n a l . c o m

Volume 20 | Issue 3 | December 2012

To promote the development of global open access to scientificinformation and research, the journal provides copyrights of allonline published papers (except where otherwise noted) for free useof readers, scientists, and institutions (such as link to the content orpermission for its download, distribution, printing, copying, andreproduction in any medium, without any changing and except thecommercial purpose), under the terms of CC BY-NC-ND 3.0 License(www.creativecommons.org/licenses/by-nc-nd/3.0), provided theoriginal work is cited. To get permission for commercial purposeplease contact the publisher.

Conflicts of Interest

The authors should disclose all issues concerning financial relationship,conflict of interest, and competing interest that may potentially influ-ence the results of the research or scientific judgment. All financial con-tributions or sponsorship, financial relations, and areas of conflict ofinterest should be clearly explained in the cover letter to the Editor-in-Chief at the time of submission, with full assurance that any relateddocument will be submitted to the journal when requested. For thedetails of journal's "Conflicts of Interest Policy" please visit www.peri-nataljournal.com.

Publication InfoOwnership: On behalf of the Perinatal Medicine FoundationCihat fien

Managing Editor: Prof. Dr. Murat Yayla

Administrative Office: Cumhuriyet Cad. 30/5 Elmada¤, Taksim34367 ‹stanbul

Due the Press Law of Turkish Republic dated as June 26, 2004 andnumbered as 5187, this publication is classified as a local periodi-cal. Perinatal Journal is published by Deomed Publishing (Copyright© 2012, Perinatal Medicine Foundation).

Publication Coordinator: ‹lknur DemirelEnglish Editor: Fikret YeflilyurtGraphic Design: Tolga Erbay Page Layout: Nurgül ÖzcanPress: Birmat Matbaac›l›k, Yüzy›l Mahallesi MASS‹T 1. Cad. No:131 Ba¤c›lar, ‹stanbul, Tel: (0212) 629 05 59-60

Printed on acid-free paper (August 2012).

DescriptionPerinatal Journal, the official publication of Perinatal Medicine Foundation, Turkish Perinatology Society and Turkish Society of Ultrasound in Obstetrics and Gynecology, is an international online open access peer-reviewed scientific journal (e-ISSN 1305-3124) published triannually in English. The manuscripts which are accept-ed for publication in the Perinatal Journal are published as a parallel publication of Turkish version in “Perinatoloji Dergisi” (p-ISSN:1300-5251, e-ISSN:1305-3132). Translation in to Turkish language is pro-vided by the publisher as free of charge for authors. This is automat-ically accepted by the authors of manuscripts at the time of submis-sion.

The journal mainly includes original clinical and experimental research articles, case reports, reviews, editorial and opinion articles, and a letters column. Perinatal Journal is can be read by perinatolo-gists, obstetricians, gynecologists, radiologists, pediatricians, sonog-raphers, midwives, radiographers, and scientific members of other related areas.

Aim and Scope Perinatal Journal aims to create an interdisciplinary scientific plat-form for sharing and discussing topics on perinatology and to share its experience with international scientific community.

CopyrightPeriantal Journal does not officially agree with the ideas of manu-scripts published in the journal and does not guarantee for any prod-uct or service advertisements in its content. Scientific and legal responsibilities of published manuscripts belong to their authors. Materials such as pictures, figures, tables etc. sent with manuscripts should be original or written approval of copyright holder should be sent with manuscript for publishing together if they were published before.

All published materials will become the sole property of, and will be copyrighted by Perinatal Journal. Therefore, "Acknowledgement of Authorship and Transfer of Copyright Agreement" are requested in addition to manuscripts that are to be assessed. Acknowledgement of Authorship and Transfer of Copyright Agreement form is available online at www.perinataljournal.com. No payment is done for manuscripts under the name of copyright or others approved for publishing in the journal and no publication cost is charged; however, reprints are at authors’ cost.

Deomed PublishingSarayard› Cad. Cemhan-Do¤an ‹fl Merkezi No: 100/16 HasanpaflaKad›köy 34722 IstanbulTelefon: +90 216 414 83 43 (Pbx) Fax: +90 216 414 83 42e-mail: [email protected] • www.deomed.com

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www.perinataljournal.com

The Official Publication of Perinatal Medicine Foundation, Turkish Perinatology Societyand Turkish Society of Ultrasound in Obstetrics and Gynecology

EditorsCihat fien,

Istanbul, Turkey

Murat Yayla, Istanbul, Turkey

Advisory BoardArif Akflit, Eskisehir, TurkeyAris Antsaklis, Athens, GreeceOlufl Api, Istanbul, TurkeySaadet Arsan, Ankara, TurkeyAbdel-Latif Ashmaig, Khartoum, SudanAbdallah Adra, Beirut, LebanonAhmet Baschat, Baltimore, MD, USAYeflim Baytur, Manisa, TurkeyAna Bianchi, Montevideo, UruguayLous Cabero-Roura, Barcelona, SpainManuel Carrapato, Porto, PortugalJose M. Carrera, Barcelona, SpainJulene Carvalho, London, UKRabihChaoui, Berlin, GermanyFrank Chervenak, New York, NY, USAEbru Çelik, Malatya, TurkeyVincenzo D’Addario, Bari, ItalyNur Daniflmend, Istanbul, TurkeyJan Deprest, Leuven, BelgiumEbru Dikensoy, Gaziantep, TurkeyGönül Dinç, Manisa, TurkeyGian Carlo DiRenzo, Perugia, ItalyTony Duan, Shanghai, ChinaJoachim Dudenhausen, Berlin, GermanyAlaa Ebrashy, Cairo, EgyptAli Ergün, Ankara, TurkeyUlrich Gembruch, Bonn, GermanyAnne Greenough, London, UKGökhan Göynümer, Istanbul, TurkeyArif Güngören, Antakya, Turkey

Davor Jurkovic, London, UKAyfle Kafkasl›, ‹stanbul, TurkeyOliver Kagan, Tübingen, GermanyÖmer Kandemir, Ankara, Turkey‹schiro Kawabata, Osaka, Japan Selahattin Kumru, Düzce, TurkeyAs›m Kurjak, Zagrep, CroatiaNilgün Kültürsay, Izmir, TurkeyMalcome Levene, Leeds, UKNarendra Malhotra, Agra, Uttar Pradesh, IndiaGiampaolo Mandruzzato, Trieste, ItalyAlexandra Matias, Porto, PortugalRatko Matijevic, Zagrep, CroatiaIsrael Meizner, Tel Aviv, IsraelMohammed Momtaz, Cairo, EgyptGiovanni Monni, Cagliari, ItalyErcüment Müngen, Istanbul, TurkeyKypros Nicolaides, London, UKLütfü Öndero¤lu, Ankara, TurkeySoner Öner, Izmir, TurkeyOkan Özkaya, Isparta, TurkeyAlexander Papitashvilli, Tbilisi, Georgia‹brahim Polat, Istanbul, TurkeyRitsuko Pooh, Osaka, JapanRuben Quintero, Tampa, FL, USANebojsa Radunovic, Belgrade, SerbiaGuiseppe Rizzo, Roma, ItalyRoberto Romero, Detroit, MI, USAHaluk Sayman, Istanbul, TurkeyElif Gül Yapar Eyi, Ankara, Turkey

The Official Publication of Perinatal Medicine Foundation, Turkish Perinatology Society and Turkish Society of Ultrasound in Obstetrics and Gynecology

Correspondence: Perinatal Journal, Perinatal Medicine Foundation,Cumhuriyet Cad. 30/5 Elmada¤, Taksim 34367 ‹stanbul, TurkeyPhone: (0212) 225 52 15 • Fax: (0212) 296 20 16 e-mail: [email protected]

Names are in alphabetical order.


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Perinatal Journalii

Coverage

The manuscripts should be prepared for one of the following article categorieswhich are peer-reviewed:

• Clinical Research Article• Experimental Study• Case Report• Technical Note• Letter to the Editor

In addition, the journal includes article categories which do not require a peerreview process but are prepared by the Editorial Board or consist of invited arti-cles, titled as:

• Editorial• Viewpoint Article (Buna Opinion Paper da diyebiliriz)• Review Article • Abstracts• Announcements• Erratum

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Following the initial review, manuscripts which have been accepted forconsideration are reviewed by at least two reviewers. The Editors of the journaldecide to accept or reject the manuscript considering the comments of thereviewers. They are authorized to reject or revise the manuscript, to suggestrequired corrections and changes upon the comments and suggestions ofreviewers, and/or to correct or condense the text by permission of the corre-sponding author. They have also the right to reject a manuscript after authors’revision. Author(s) should provide additional relevant data, documents, or infor-mation upon the editorial request if necessary.

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All manuscripts presenting data obtained from studies involving human subjectsmust include a statement that the written informed consent of the participantswas obtained and that the study was approved by an institutional ethics boardor an equivalent body. This institutional approval should be submitted with themanuscript. Authors of case reports must submit the written informed consentof the subject(s) of the report or of the patient’s legal representatives for thepublication of the manuscript. All studies should be carried out in accordancewith the World Medical Association Declaration of Helsinki, covering the latestrevision date. Patient confidentiality must be protected according to the univer-sally accepted guidelines and rules. Manuscripts reporting the results of experi-mental studies on animals must include a statement that the study protocol wasapproved by the animal ethics committee of the institution and that the studywas conducted in accordance with the internationally accepted guidelines,including the Universal Declaration of Animal Rights, European Convention forthe Protection of Vertebrate Animals Used for Experimental and Other ScientificPurposes, Principles of Laboratory Animal Science, and the Handbook for theCare and Utilization of Laboratory Animals. The authors are strongly requestedto send the approval of the ethics committee together with the manuscript. Inaddition, manuscripts on human and animal studies should describe proceduresindicating the steps taken to eliminate pain and suffering.

Yazarlar ayr›ca, çal›flma ile ilgili bilinmesi gereken herhangi bir mali iliflkiyi yada ç›kar çak›flmas› (conflict of interest) veya rekabet (competing interest) alanlar›n›aç›klamakla yükümlüdürler. Çal›flmaya yap›lan tüm mali katk›lar ya da sponsor-luklar, çal›flmayla ilgili olabilecek mali iliflkiler ya da kiflisel örtüflme konular› yay›-n›n gönderildi¤i s›rada baflvuru mektubunda belirtilmelidir. Derginin Ç›kar Çak›fl-mas› Politikas› ile ilgili ayr›nt›l› bilgiyi de içeren ve olas› ç›kar çak›flmas› durumundakullan›labilecek Ç›kar Çak›flmas› Beyan Formu için bkz. www.perinataldergi.com.

The authors should also disclose all issues concerning financial relationship,conflict of interest, and competing interest that may potentially influence theresults of the research or scientific judgment. All financial contributions or spon-sorship, financial relations, and areas of conflict of interest should be clearlyexplained in the cover letter to the Editor-in-Chief at the time of submission,with full assurance that any related document will be submitted to the journalwhen requested. For the details of journal's "Conflict of Interest Policy" pleaseread the PDF document which includes "Conflicts of Interest DisclosureStatement".

Perinatal Journal follows the ethics flowcharts developed by the Committeeon Publication Ethics (COPE) for dealing with cases of possible scientific miscon-duct and breach of publication ethics. For detailed information please visitwww.publicationethics.org.

Manuscript Preparation In addition to the rules listed below, manuscripts to be published in PerinatalJournal should be in compliance with the Uniform Requirements forManuscripts Submitted to Biomedical Journals published by InternationalCommittee of Medical Journal Editors (ICMJE) of which latest version is availableat www.icmje.org.

Authors are requested to ensure that their manuscript follows the appro-priate guidelines such as CONSORT for randomized controlled trials, STROBE forobservational studies, STARD for diagnostic accuracy studies, and PRISMA forsystematic reviews and meta-analyses, for the study design and reporting ifapplicable.

Authorship and Length of TextsThe author(s) must declare that they were involved in at least 3 of the 5 stagesof the study stated in the “Acknowledgement of Authorship and Transfer ofCopyright Agreement” as “designing the study”, “collecting the data”, “ana-lyzing the data”, “writing the manuscript” and “confirming the accuracy of thedata and the analyses”. Those who do not fulfill this prerequisite should not bestated as an author.

Original research articles base on clinical or experimental studies. Themain text should not exceed 2500 words (max. 16 pages) and there should bea maximum 6 authors

Case reports should illustrate interesting cases including their treatmentoptions. The main text should not exceed 2000 words (max. 8 pages) and thereshould be a maximum 5 authors.

Viewpoint articles: Only by invitation and should be no more than 2000words long (max. 8 pages).

Review articles: Only by invitation and should be no more than 4000-5000 words long (max. 20 pages).

Technical notes aims to present a newly diagnostic or therapeuticmethod. They should not exceed 2000 words (max. 8 pages) and include a max-imum of 10 references.

Letters to the Editor should be no more than 500 words long (max. 2pages) and include a maximum of 10 references.

Sections in the ManuscriptsManuscripts should be designed in the following order: title page, abstract,main text, references, and tables, with each typeset on a separate page:

Page 1 - Title pagePage 2 - Abstract and key wordsPage 3 and next - Main textNext Page - ReferencesNext Page - Table heading and tables (each table should be placed in sep-

arate pages)Next Page - Figure legends and figures (each figure should be placed in

separate pages)Last Page - Appendices (patient forms, surveys etc.)

Title pageThis page should only include the title of the manuscript, which should be care-fully chosen to better reflect the contents of the study. No anusual abbreviationsshould be used in the title of the manuscript. A short title as running heading

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Voulume 20 | Issue 3 | December 2012 iii

Instructions for the Authorswww.perinataljournal.com

not exceeding 40 characters should be given which is desired to appear on toppart of continuing pages when journal is published.

Abstract page

Abstracts should not contain any abbreviation and references. They should beprepared under following designs.

— Abstracts of research articles should be max. 250 words and struc-tured in four paragraphs using the following subtitles: Objective, Methods,Results, and Conclusion. Following the abstract, each abstract page shouldinclude max. 5 key words separated with comma and written in lower cases.

— Abstracts of case reports should be max. 125 words and structured inthree paragraphs using the following subtitles: Objective, Case, Conclusion.Following the abstract, each abstract page should include max. 3 key words sep-arated with comma and written in lower cases.

— Abstracts of review articles should be max. 300 words and presentednot structured in one paragraph. Following the abstract, each abstract pageshould include max. 5 key words separated with comma and written in lowercases.

— Abstracts of technical notes should be max. 125 words and structuredin three paragraphs using the following subtitles: Objective, Technique,Conclusion. Following the abstract, each abstract page should include max. 3key words separated with comma and written in lower cases.

Main text:The sections in main text are defined according to the manuscript type.

— In research articles, main text should consist of sections titled as"Introduction, Methods, Results, Discussion and Conclusion". Each title mayhave subtitles. The categories of subtitles should be clearly defined.

The Introduction section should include a brief summary of the base of thework and clearly states the purpose of the study.

The Methods section should contain a detailed description of the material,the study design and clinical and laboratory tests, and statistical methods used.A statement regarding the ethical issues should also be given in this section.

The Results section should provide the main findings of the study. Datashould be concisely presented, preferably in tables or graphs.

The Discussion section should mainly rely on the results derived from thestudy, with relevant citations from the most recent literature.

The Conclusion section should briefly and claearly present the conclusionsderived from the results of the study. It should be in compliance with the aim ofthe work and and point out its application in clinical practice.

— In Case Reports, main text should be divided with the titles"Introduction, Case(s), Discussion". Reported case(s) should be introducedclearly including the case story, and the results of laboratory tests should begiven in table format as far as possible.

— The text of the reviews articles should follow the "Introduction" andbe organized under subtitles which should clearly define the text's context cat-egorization. The Reviews are expected to include wide surveying of literatureand reflect the author's personal experiences as far as possible.

— The text of the technical note type of articles should be divided into"Introduction, Technic, Discussion". The presented technic should be definedbriefly under the related title, and include illustrations or figures as soon as pos-sible.

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References

References used in the text should be directly related to the topic, as recent aspossible and in enough numbers. They should be numbered in square bracketsin the order in which they are mentioned in the text including Tables andFigures. Citation order should be checked carefully.

Only published articles or articles in press can be used in references.Unpublished data including conference papers or personal communicationsshould not be used. Papers published in only electronic journals or in the

preprint or online first issues of the electronic versions of conventional periodi-cals should be absolutely presented with DOI (digital object identifier) numbers.

Journal titles should be abbreviated according to the Index Medicus. Allauthors if six or fewer should be listed; otherwise, the first six and “et al.”should be written.

Direct use of references is strongly recommended and the authors may beasked to provide the first and last pages of certain references. Publication of themanuscript will be suspended until this request is fulfilled by the author(s).

The style and punctuation should follow the formats outlined below:

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

— Article published in an only electronic journal: Lee J, Romero R, XuY, Kim JS, Topping V, Yoo W, et al. A signature of maternal anti-fetal rejectionin spontaneous preterm birth: chronic chorioamnionitis, anti-human leukocyteantigen 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: Gleicher N,editors. Principles and practice of medical therapy in pregnancy. 3rd ed. NewYork: Appleton&Lange; 1998. p. 1022-7.

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All illustrations (photographs, graphics, and drawings) accompanying the man-uscript should be referred to as “figure”. All figures should be numbered con-secutively and mentioned in the text. Figure legends should be added at the endof the text as a separate section. Each figure should be prepared as a separatedigital file in “jpeg” format, with a minimum 300 dpi or better resolution. Allillustrations should be original. Illustrations published elsewhere should be sub-mitted with the written permission of the original copyright holder. For recog-nizable photographs of human subjects, written permission signed by thepatient or his/her legal representative should be submitted; otherwise, patientnames or eyes must be blocked out to prevent identification. Microscopic pho-tographs should include information on staining and magnification.

Each table should be prepared on a separate page with table heading ontop of the table. Table heading should be added to the main text file on a sep-arate page when a table is submitted as a supplementary file.

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For a swift peer review, Perinatal Journal operates a web-based submission, peerreview and manuscript tracking system. Authors are required to submit theirarticles online. Details of how to submit online can be found at www.perina-taljournal.com.

Submission Checklist

The following list will be useful during the final check of a manuscript beforesubmission:

1. Manuscript length (max. 4000 words for research articles)

2. Number of authors (max. 6 authors for research articles)

3. Title page (no anusual abbreviations)

4. Abstracts (max. 250 words for research articles)

5. Key words (max. 5 keys for research articles)

6. Main text (subtitles)

7. References (listed according to the rules of ICMJE)

8. Figures and tables (numbering; legends and headings; copyrightinfo/permission)

9. Cover letter

10. Acknowledgement of Authorship and Transfer of CopyrightAgreement (undersigned by all authors)

11. Conflicts of Interest Disclosure Statement (if necessary)

Voulume 20 | Issue 3 | December 2012 v

Research Articles

The impact of fetal inflammatory response syndrome on perinatal outcomes in cases of preterm premature rupture of membranes | 121

Fetal inflamatuar yan›t sendromunun preterm erken membran rüptürü olgular›n›n perinatal sonuçlar› üzerine etkisi

Orkun Çetin, ‹pek Dokurel Çetin, Onur Güralp, Cihat fien, Seyfettin Uluda¤, Ali Galip Zebitay

Evaluation of prenatal care in Istanbul: a population based study | 126‹stanbul’da do¤um öncesi bak›m hizmetlerinin de¤erlendirilmesi: Toplum tabanl› bir araflt›rmaBinali Çatak, Hatice ‹ki›fl›k, Savafl Baflar Kartal, Can Öner, Handan Hazal Uluç, Özgür Se¤men

Retrospective analysis of stillbirth cases in a regional hospital | 135Bir bölge hastanesinde ölü do¤um olgular›n›n retrospektif analiziMuhammet Erdal Sak, Mehmet S›dd›k Evsen, Hatice Ender Soydinç, Sibel Sak, Serdar Baflarano¤lu, Ahmet Yal›nkaya

Investigation of the relationship between levels of oxidative stress markers in the second trimester amniotic fluid with preeclampsia and preterm delivery | 140

‹kinci trimesterde amniyotik s›v›da oksidatif stres belirteçlerinin düzeyleri ile preeklampsi geliflimi ve erken do¤um aras›ndaki iliflkinin araflt›r›lmas›Ebru Çelik, Abdullah Karaer, Ercan Y›lmaz, Ilg›n Türkçüo¤lu, Önder Çelik, Yavuz fiimflek, P›nar K›r›c›, Elif Özerol, Kevser Tanbek

Case Reports

Ovarian cyst rupture during real-time transvaginal Doppler ultrasonography | 146Gerçek zamanl› transvajinal Doppler ultrasonografi esnas›nda over kist rüptürüMekin Sezik

Agenesis of ductus venosus: a case report | 150Ductus venosus agenezisi: Olgu sunumuUmut Kutlu Dilek, Burcu Dilek

Sonographically documented spontaneous resolution of isolated fetal ascites | 153Ultrasonografik izlemde spontan remisyona u¤rayan izole fetal asit olgu sunusufiad›man K›ykaç Alt›nbafl, Ömer Kandemir, Serdar Yalvaç, Ümit Göktolga

Interhemispheric arachnoid cyst associated with meningomyelocele: a case report | 156Meningomiyeloselin efllik etti¤i interhemisferik araknoid kist: Olgu sunumu Resul Ar›soy, Emre Erdo¤du, Oya Demirci, Oya Pekin, P›nar Kumru, Semih Tu¤rul

Bilateral type 1 congenital cystic adenomatoid malformation: a case report | 160Bilateral Tip 1 konjenital kistik adenomatoid malformasyon: Olgu sunumuResul Ar›soy, Emre Erdo¤du, Oya Pekin, Oya Demirci, P›nar Kumru, Semih Tu¤rul

Index

Subject, author and reviewer indexes | 164

ContentsVolume 20, Issue 3, December 2012


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The impact of fetal inflammatory response syndromeon perinatal outcomes in cases of preterm premature

rupture of membranesOrkun Çetin3, ‹pek Dokurel Çetin2, Onur Güralp1, Cihat fien1, Seyfettin Uluda¤1, Ali Galip Zebitay3

1Department of Obstetrics and Gynecology, Cerrahpafla Medical Faculty, Istanbul University, Istanbul, Turkey2Department of Pediatrics, Cerrahpafla Medical Faculty, stanbul University, Istanbul, Turkey

3Department of Obstetrics and Gynecology, Süleymaniye Maternity Training and Research Hospital, Istanbul, Turkey

Abstract

Objective: To evaluate the impact of fetal inflammatory responsesyndrome (FIRS) in the cases of preterm premature rupture ofmembranes (PPRM). Methods: The study was designed prospectively. The study wasconsisted of 40 cases between 26 and 37 weeks gestation diagnosedas PPRM without any obstetric and maternal pathologic findings.All cases were followed-up by hospitalization. Umbilical cord sam-pling was done for IL-6 levels at the time of delivery. The perina-tal outcomes of the cases were recorded after birth.Results: Forty PPRM cases were followed-up in our study. Themean gestational week of cases at the time of delivery was33.5±3.19. The mean 1st and 5th minutes Apgar scores of thecases with FIRS were 4.6 and 6.2, respectively. The mean 1st and5th minutes Apgar scores of the cases without FIRS were 6.9 and8.3, respectively. There was a statistically significant reverse cor-relation between IL-6 levels of umbilical cord blood and 1st and5th minutes Apgar scores in PPRM cases (p<0.01). There was alsostatistically significant reverse correlation between IL-6 levels ofumbilical cord blood and birth weight (p<0.01).Conclusion: Checking IL-6 level of umbilical cord blood (higherthan 11 pg/ml) made it easy to diagnose FIRS. Umbilical cordblood sampling at delivery for IL-6 level is not a prenatally diag-nostic test but if we can diagnose FIRS earlier, we have a chanceto gain time for preparing more appropriate intervention condi-tions in order to protect newborn against the complications thatmay develop associated with neonatal sepsis and proinflammatorycytokines.

Key words: Fetal inflammatory response syndrome, preterm pre-mature rupture of membranes, perinatal outcomes.

Fetal inflamatuar yan›t sendromunun preterm erkenmembran rüptürü olgular›n›n perinatal sonuçlar›üzerine etkisiAmaç: Preterm erken membran rüptürü (PEMR) olgular›nda, fe-tal inflamatuar yan›t sendromunun (FIRS) perinatal sonuçlar üze-rine olan etkisini araflt›rmak.Yöntem: Çal›flma prospektif bir araflt›rma olarak planland›. Çal›fl-maya 26.-37. gestasyonel hafta aras›ndaki obstetrik ve maternalpatolojik bulgusu olmayan 40 preterm erken membran rüptürüolan gebe dahil edildi. Bütün hastalar hastaneye yat›r›larak takipedildi. Do¤umu takiben tüm hastalardan kordon kan› al›narak IL-6 seviyesi çal›fl›ld›. Do¤um sonras›nda olgular›n perinatal sonuçla-r› kay›t alt›na al›nd›. Bulgular: Çal›flmam›zda, PEMR olan 40 olgu klinik gebelik taki-bine al›nd›. Olgular›n ortalama do¤um haftas› ise 33.5±3.19 idi.FIRS geliflen olgular›n ortalama 1. dakika Apgar skorlar› 4.6 iken;5. dakika Apgar skorlar› 6.2 bulundu. FIRS geliflmeyen olgular›n 1.dakika Apgar skorlar› 6.9 iken; 5. dakika Apgar skorlar› 8.3 olarakbulundu. PEMR olgular›n›n, umbilikal kordon kan› IL-6 düzeyiile 1. ve 5. dakika Apgar skorlar› aras›nda istatistiksel olarak anlam-l› ters korelasyon oldu¤u saptand› (p<0.01). Umbilikal kordon ka-n› IL-6 düzeyi ile olgular›n do¤um tart›lar› aras›nda istatistikselolarak anlaml› ters yönde korelasyon oldu¤u tespit edildi (p<0.01). Sonuç: Çal›flmam›zda, umbilikal kordon kan›nda bakt›¤›m›z IL-6düzeyinin bak›lmas› (11 pg/ml üzeri), FIRS tan›s›n›n konulmas›n›kolaylaflt›rm›flt›r. Do¤umda umbilikal kord kan›nda IL-6 düzeyitayini; prenatal bir tan› testi olmasa da FIRS tan›s›n›n erken konul-mas› sayesinde, yenido¤an döneminde, neonatal sepsise ve proinf-lamatuar sitokinlere ba¤l› geliflebilecek komplikasyonlara karfl› da-ha uygun müdahale koflullar›n›n haz›rlanabilmesi için zaman kaza-n›lmas›n› sa¤layacakt›r. Anahtar sözcükler: Fetal inflamatuar yan›t sendromu, pretermerken membran rüptürü, perinatal sonuçlar.

Correspondence: Orkun Çetin, MD. Süleymaniye Do¤umevi E¤itim ve Araflt›rma Hastanesi. Telsiz Mah. Kazl›çeflme, Istanbul, Turkey.e-mail: [email protected]

Received: May 21, 2012; Accepted: September 7, 2012

©2012 Perinatal Medicine Foundation

Available online at:www.perinataljournal.com/20120203004

doi:10.2399/prn.12.0203004QR (Quick Response) Code:

Research Article

Perinatal Journal 2012;20(3):121-125

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IntroductionFetal infection and excessive inflammatory cytokineresponse increases neonatal morbidity. The spreadingways of infection can be ascending (from vagina to cervixand cavity), hematogenous (through placenta), intraab-dominal (through oviducts), and iatrogenic (duringamniocentesis). Fetal vasculitis is defined as the presenceof neutrophiles on the chorion (chorionic vasculitis) andumbilical cord (funisitis-umbilical vasculitis) vessel walls.Fetal vasculitis is one of the most essential componentsof fetal inflammatory response. Maternal leucocytes mayinvade umbilical cord by passing from intervillous gap tochorionic surface, and from here passing to amnion andamniotic fluid. Funisitis is associated with endotheliumactivation which has a key role in multi-organ dysfunc-tion.[1,2] It is also associated with bad neonatal outcomessuch as increased neonatal sepsis, late period bron-chopulmonary dysplasia.[3]

Fetal inflammatory response syndrome (FIRS) hasshort- and long-term impacts on neonatal morbidity.Its short-term impacts are: (1) periventricular leuko-malacia (PVL), (2) intraventricular hemorrhage (IVH),(3) fetal sepsis, pneumonia, and (4) necrotizing entero-colitis. In the long-term, it is associated with a numberof fetal and neonatal morbidities such as cerebral palsy(CP), and bronchopulmonary dysplasia (BPD).[4] In thebeginning, infection appears first, then prematurebirth risk appears as a result of inflammation.Inflammation is the part of immediate, non-specificnatural immune response. Excessive or decreasedimmune response may cause disease. If immuneresponse is insufficient, infection develops; but ifimmune response is excessive, then FIRS develops.

In the diagnosis of FIRS, fetal plasma IL-6 concen-tration above 11 pg/ml is defined as threshold value infetal inflammatory response. IL-6 levels higher than 11pg/ml are associated with neonatal morbidityincrease.[5] The diagnosis can be established by CRPanalysis in umbilical cord blood sampling.[6] The diag-nosis also can be established by white blood cell countin the amniotic fluid.[7] However, evaluating cytokinelevels in a single time period does not show sufficientincrease secondary to inflammatory response. On thatsense, it may remain incapable of revealing the associ-ation between inflammatory response and possibleneonatal morbidities. In our study, we researched theimpact of fetal inflammatory response syndrome onperinatal outcomes in cases of preterm premature rup-ture of membrane according to the literature.

MethodThe study was planned as a prospective research. Thecases included to the study were chosen among preg-nants who had premature membrane rupture whoreferred to Perinatology Clinic of the Department ofObstetrics and Gynecology, Cerrahpafla MedicalFaculty, Istanbul University between January 2009 andJuly 2011. Forty cases between 26 and 37weeks gestationdiagnosed as preterm premature rupture of membraneswithout any obstetric and maternal pathologic findingswere included to the study. Pregnants who presentedmaternal (diabetes mellitus, cardiac disease, preeclamp-sia-eclampsia, ablatio placenta, multiple pregnancy,polyhydramniosis, acute pyretic disease) and fetal (severeintrauterine growth retardation, dead fetus, near-fatalfetal anomaly) factors were excluded from the study.

The diagnosis of preterm premature rupture ofmembrane was established by observing active waterbreak during dry vaginal speculum examination con-sidering the anamnesis of the patient. In patients with-out active water break, the diagnosis was established bymaking pH analysis via vaginal litmus paper.Additionally, the diagnosis was confirmed in allpatients by carrying out single-step immunoassay test.All patients were briefed about the study by informedconsents prepared previously. All of the patients werefollowed-up for vital findings, uterine sensitivity anddaily NST by hospitalization. All patients were admin-istrated 4 gr/day ampicilin empirically. Totally 2 dosesof betamethasone were administrated intramuscularlyonce in every 12 hours to all pregnants who were below34 weeks gestation in order to provide fetal lung mat-uration. When active labor began, fetal distress wasdetected and chorioamnionitis findings were detected(maternal fever over 38°C, uterine sensitivity, mal-odorous discharge, maternal tachycardia, fetal tachy-cardia ‘at and above 160 pulse/minute’, high whiteblood cell ‘at and above 15,000 leucocyte/microliter’,increased CRP), conservative method was terminated.

In accordance with the obstetric indications, thepatients delivered by normal labor, normal labor withinduction, and cesarean. Cord blood was taken to drytube from all patients during labor. Obtained materialwas centrifuged within maximum 2 hours and serumswere kept at -33°C. Serums were processed by IL-6 kit(ELISA DIA Source). IL-6 was shaken at the roomtemperature and incubated for 2 hours and 15 minutes.

After the delivery, CRP and culture materials (bloodculture, culture of gastric aspirates) were taken from


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newborns. Neonatal sepsis diagnosis was established withclinical findings (paleness, lethargy, irritability, apnea,respiratory distress, bradycardia, tachycardia, hypoten-sion, vomiting, fever) and/or positive cultures of bloodand gastric aspirates. FIRS diagnosis was establishedwhen cord blood IL-6 concentration was above 11pg/milliliter. After delivery, labor information of thepatients (maternal age, parity, PRM time, PMR follow-up period, whether induction was performed or not,delivery type, cesarean indication, birth weight, 1st and5th minutes Apgar scores of the baby, gender of thebaby) were recorded. Percentage, mean, standard devia-tion, and minimum and maximum values were used fordefinitive analysis. If data were qualitative, chi-square,Fisher’s Chi-Square was used in comparisons. In correla-tion analysis, Spearman rank correlation was calculated.

ResultsIn our study, 40 patients with PPRM were includedinto clinical pregnancy follow-up. Mean age of ourcases was 312±5.3. While mean gravida of our caseswas 2.1±1.3, mean parity was 0.7±0.3. Mean gestation-al week of our cases at the time when PPRM developedwas 32.5±3.3 (minimum: 26.0 - maximum: 36.0). Meandelivery week of our cases was 33.5±3.19 (minimum:27.0 - maximum: 37.0). Mean follow-up period of our

cases was 5.8±2.6 day (minimum: 3.0 -maximum: 15.0).Mean birth weight of our cases was 2184.38±757.8 g(minimum: 400.0 - maximum: 3280.0). Mean 1stminute Apgar score of our cases was 5, while mean 5thminute Apgar score was 7.

There is statistically significant correlation amongIL-6, 1st minute Apgar score, 5th minute Apgar scoreand birth weight (p<0.001). There is statistically signif-icant reverse correlation among IL-6, 1st minute Apgarscore, and 5th minute Apgar, respectively 32.0% and31.0% correlation (respectively; Spearman rho: -0.32,0.31; p=0.005, p=0.006). Also there is statistically signif-icant reverse correlation between IL-6 and birthweight, which is 41.0% (Spearman rho: -0.41; p=0.003).

Consequently, Apgar scores and birth weightdecrease as IL-6 increases (Table 1). Mean 1st minuteApgar score of FIRS cases was found as 4 while 5thminute Apgar score was 6. These values were 6 and 8,respectively in cases without FIRS. Apgar scores werestatistically and significantly lower in cases FIRS com-pared to cases without FIRS (Table 2).

DiscussionAlthough Systemic inflammatory response syndromewas defined as a local phenomenon in the past, it is asystemic pathology characterized by fever, tachycardia,

Table 1. Evaluation of IL-6, birth weight, and the scores of Apgar 1 and Apgar 5.

Apgar 1 Apgar 5 Birth weight

IL- 6 Spearman Rho -0.320** -0.310* -0.410*

p 0.005 0.006 <0.001

N 40 40 40

*p<0.001

Table 2. Evaluation of the 1st minute and 5th minute Apgar scores according to the presence of FIRS.

FIRS Apgar 1 Apgar 5

N/A N 20 20

Mean 6.9000 8.3500

Standard deviation 1.77408 .98809

Available N 20 20

Mean 4.6000 6.2000

Standard deviation 2.34857 2.26181

p 0.002 0.001

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hyperventilation, and leukocytosis. There is a miscon-ception that infection or inflammation does not exist inthe non-presence of systemic findings (fever, leukocy-tosis).[13] Now, we know that histological inflammationand chorioamnionitis are sub-clinical in many casesduring term and preterm labors.

Granulocyte and macrophages have an essentialrole in natural immune response. Chemokines aresmall peptides or glycoproteins that can be solved andresponsible for communication among cells (IL, INF,TNF, growth factors and chemokines). Chemokinesenables leucocytes to migrate into inflammation region(IL-8, IL-10). Cytokines can be in proinflammatory oranti-inflammatory structure. IL- 1, IL- 6, TNF-alphaand IFN-gamma are proinflammatory cytokines; IL-4,IL-10, IL-11, and IL-13 are anti-inflammatorycytokines. Systemic inflammatory response emergingin fetus is called “fetal inflammatory response syn-drome” (FIRS). It is characterized by proinflammatorycytokines increased in amniotic fluid and fetal bloodand the presence of fetal vasculitis. There is anintrauterine infection and an excessive inflammatoryresponse appears against the infection. Intrauterineinfection affects maternal decidua, myometrium, amni-otic and chorionic membranes, amnion fluid, cord andplacenta. There are many data stating that theseintraamniotic cytokines are fetal originated. Theimpact of fetal inflammatory response on possible out-comes is more important.[1]

While IL-6 and IL-8 levels are at the highest levelsin umbilical cord blood and postnatal 6th hour, theygradually decrease and reach the lowest levels at 72ndhour. So, the time of intrauterine inflammation and theevaluation time of cytokines during postnatal periodare essential.[8] Regarding with FIRS, target organssuch as hematopoietic system, adrenal glands, kidneys,lungs, skin, and brain will be affected negatively. It wasshown in the studies performed that there[14] is anincrease in white blood cell count of newborn in thepresence of histological chorioamnionitis and placentalinflammation in the cases of preterm premature rup-ture of membrane (above 24 hours).[15,16] This wasexplained by the increase in IL-6 level.[17] Detectinghigh level of IL-6, which is a proinflammatorycytokine, in umbilical cord blood was considered asassociated with bad perinatal outcomes.[18,19]

In our study, IL-6 levels in umbilical cord bloodwas found as reverse correlated with 1st and 5th min-

utes Apgar scores and birth weight. It was observedthat both 1st and 5th minutes Apgar scores, and birthweight decreased as IL-6 level increased. When thecases with and without FIRS were compared, Apgarscores were particularly low in cases with FIRS.

In the follow-up of PPRM cases, serial white bloodcell count and C-reactive protein (CRP) measurementsare used together with basal and weekly vaginal cul-tures in the follow-up of chorioamnionitis develop-ment. Carrying out amniocentesis against the possibil-ity of secret chorioamnionitis is controversial and thereis no sufficient experience.[9] In the limited number ofstudies performed, the association of proinflammatorycytokines (IL-6, IL-8, IL-18) and microbial invasion ofamniotic cavity in PPRM cases. In our study, FIRSdiagnosis was clearly established by means of IL-6 level(above 11 pg/ml) we checked in umbilical cordblood.[5,6] Umbilical cord blood sampling at delivery forIL- 6 level is not a prenatally diagnostic test but if wecan diagnose FIRS earlier, we have a chance to gaintime for preparing more appropriate intervention con-ditions in order to protect newborn against the compli-cations that may develop associated with neonatal sep-sis and proinflammatory cytokines (newborn intensecare unit, antibiotic prophylaxis). By evaluating levelsof other proinflammatory cytokines (such as IL-1,TNF-alpha) like IL-6, more successful perinatal out-comes can be obtained in FIRS cases.

The studies performed in recent years make us tothink that fetal inflammatory response syndrome aris-ing due to proinflammatory cytokines and complica-tions related with this condition such as intraventricu-lar hemorrhage, periventricular leukomalacia and cere-bral palsy cannot be prevented only by antibiotic treat-ment. Animal testings which used anti-inflammatoryand chemical agents for the effects of IL-1 and IL-6widened horizons.[10-12] These treatments can be com-bined with regimes used to prevent or treat fetal mor-bidity cause by intrauterine infection and inflammationassociated with PPRM.

ConclusionProspective and new studies with wider scale are need-ed in order to understand the etiology of fetal inflam-matory response syndrome and to prevent its compli-cations.

Conflicts of Interest: No conflicts declared.

References1. Ugwumadu A. Infection and fetal neurologic injury. Curr

Opin Obstet Gynecol 2006;18:106-11. 2. D'Alquen D, Kramer BW, Seidenspinner S, Marx A, Berg

D, Groneck P, et al. Activation of umbilical cord endothelialcells and fetal inflammatory response in preterm infants withchorioamnionitis and funisitis. Pediatr Res 2005;57:263- 9.

3. Yoon BH, Romero R, Park JS, Kim M, Oh SY, Kim CJ, etal. The relationship among inflammatory lesions of theumbilical cord (funisitis), umbilical cord plasma interleukin 6concentration, amniotic fluid infection, and neonatal sepsis.Am J Obstet Gynecol 2000;183:1124-9.

4. Gomez R, Romero R, Edwin SS, David C. Pathogenesis ofpreterm labor and preterm premature rupture of membranesassociated with intraamniotic infection. Infect Dis ClinNorth Am 1997;11:135-76.

5. Gomez R, Romero R, Ghezzi F, Yoon BH, Mazor M, BerrySM. The fetal inflammatory response syndrome. Am JObstet Gynecol 1998;179:194-202.

6. Yoon BH, Romero R, Shim JY, Shim SS, Kim CJ, Jun JK.C-reactive protein in umbilical cord blood: a simple andwidely available clinical method to assess the risk of amniot-ic fluid infection and funisitis. J Matern Fetal Neonatal Med2003;14:85-90.

7. Sampson JE, Theve RP, Blatman RN, Shipp TD, BianchiDW, Ward BE, et al. Fetal origin of amniotic fluid polymor-phonuclear leukocytes. Am J Obstet Gynecol 1997;176(1 Pt1):77-81.

8. Dammann O, Leviton A. Brain damage in preterm new-borns: biological response modification as a strategy toreduce disabilities. J Pediatr 2000;136:433- 8.

9. Dudley J, Malcolm G, Elwood D. Amniocentesis in themanagement of preterm premature rupture of the mem-branes. Aust N Z J Obstet Gynecol 1991;31:331-6.

10. Kenyon S, Boulvain M, Neilson J. Antibiotics for pretermrupture of membranes. Cochrane Database Syst Rev2003;(2):CD001058.

11. Murphy DJ, Sellers S, MacKenzie IZ, Yudkin PL, JohnsonAM. Case-control study of antenatal and intrapartum riskfactors for cerebral palsy in very preterm singleton babies.Lancet 1995;346:1449-54.

12. Spinillo A, Capuzza E, Stronati M. Effect of preterm prema-ture of membranes on neurodevelopmental outcome: followup at two years of age. Am J Obstet Gynecol 1995;102:882-7.

13. Kiflniflci H, Gökflin E, Durukan T, Üstay K, Ayhan A,Gürgan T, Öndero¤lu LS.Temel kad›n hastal›klar› vedo¤um bilgisi. Ankara: Nobel; 1996. p. 1465-80.

14. Mandel D, Oron T, Mimouni GS, Littner Y, Dollberg S,Mimouni FB. The effect of prolonged rupture of mem-branes on circulating neonatal nucleated red blood cells. JPerinatol 2005;25:690-3.

15. Leikin E, Garry D, Visintainer P, Verma U, Tejani N.Correlation of neonatal nucleated red blood cell counts inpreterm infants with histologic chorioamnionitis. Am JObstet Gynecol 1997;177:27-30.

16. Dulay AT, Buhimschi IA, Zhao G, Luo G, Abdel-Razeq S,Cackovic M, et al. Nucleated red blood cells are a directresponse to mediators of inflammation in newborns withearly-onset neonatal sepsis. Am J Obstet Gynecol2008;198:426-9.

17. Jones SA. Direct transition from innate to acquired immuni-ty: defining a role for IL-6. J Immunol 2005;175:3463-8.

18. Viscardi RM, Muhumuza CK, Rodriguez A, Fairchild KD,Sun CC, Gross GW, et al. Inflammatory markers inintrauterine and fetal blood and cerebrospinal fluid compart-ments are associated with adverse pulmonary and neurolog-ic outcomes in preterm infants. Ped Res 2004;55:1009-17.

19. Yoon BH, Park CW, Chaiworapongsa T. Intrauterine infec-tion and the development of cerebral palsy. BJOG 2003;110Suppl 20:124-7.


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Evaluation of prenatal care in Istanbul: a populationbased study

Binali Çatak1, Hatice ‹ki›fl›k2, Savafl Baflar Kartal3, Can Öner4, Handan Hazal Uluç5, Özgür Se¤men4

1Ministry of Health, Üsküdar Public Health Center, Istanbul, Turkey2Ministry of Health, Ümraniye Public Health Center, Istanbul, Turkey

3Ministry of Health, Istanbul Public Health Department, Istanbul, Turkey4Ministry of Health, Pendik Public Health Center, Istanbul, Turkey5Ministry of Health, Kartal Public Health Center, Istanbul, Turkey

Abstract

Objective: Prenatal care (PC) is one of the most important factorshaving effects on both maternal and infant health. The aim of thisstudy is to evaluate the prenatal care that is provided by both fam-ily physicians and obstetricians. Methods: The study population of this cross sectional study com-posed of 99,254 women whose pregnancies was recorded by theirfamily physicians (FP) on November 27th, 2011 in Istanbul. 1454 ofthese pregnant women were randomly selected and included in thestudy. All data were collected by means of a questionnaire. 94.0% ofthe study population was reached. Values of percentage, frequency,mean, and median were used for data analysis.Results: Evaluation of delivered women showed that 12.3% gotprenatal care from a FP, 3.5% from an obstetrician and 1.3% didnot get any PC. Among delivered women who had made four ormore visits for PC, 53.3% of them received this service from a FPand 89.0% of them from an obstetrician. 74% of pregnant womenget PC service from FP and %94 of them from obstetrician withinfirst 14 weeks. Among pregnants who received PC from FP, bloodpressure was measured in 96% of them, weight gain was measuredin 92.5% of them, and 25.1% of them was auscultated for cardiacsounds. On the other hand, among pregnants who received PCfrom obstetrician, blood pressure was measured in 95.4% of them,weight gain was measured in 91.8% of them, ultrasonographyexamination was performed in 98.2% of them, blood analysis wasdone in 90% of them, and family planning consultancy was provid-ed to 31.5% of them.Conclusion: It is shown that although the amount of PC provid-ed in Istanbul was adequate, the quality was unsatisfactory.Therefore, regular and frequent on-the-job training for healthpersonnel should be organized and the PC program of theMinistry of Health should actively be provided.Key words: Prenatal care, family physician, obstetrician, Istanbul.

‹stanbul’da do¤um öncesi bak›m hizmetlerininde¤erlendirilmesi: Toplum tabanl› bir araflt›rma Amaç: Do¤um öncesi bak›m (DÖB) gebe ve bebek sa¤l›¤› aç›s›n-dan önemli unsurlardan birisidir. Araflt›rmada ‹stanbul il düzeyin-de aile hekimleri ve kad›n do¤um uzmanlar›nca verilen DÖB hiz-metlerinin de¤erlendirilmesi amaçlanm›flt›r.Yöntem: Kesitsel tipte yap›lan araflt›rman›n evrenini ‹stanbul’da27 Kas›m 2011 tarihinde aile hekimlerine kay›tl› 99.254 gebe olufl-turmufltur. Örnekleme al›nacak gebe say›s› 1454 olarak hesaplan-m›fl ve al›nacak gebeler randomizasyonla belirlenmifltir. Veriler,haz›rlanan soru formu ile toplanm›flt›r. Örneklemin %94’üne ula-fl›lm›flt›r. Verilerin analizinde yüzde, frekans, ortalama ve ortancakullan›lm›flt›r.Bulgular: Do¤um yapm›fl gebelerin %12.3’ü aile hekiminden,%3.5’i kad›n do¤um uzman›ndan ve %1.3’ü ise hiçbir sa¤l›k per-sonelinden DÖB almam›flt›r. 4 ve daha fazla DÖB alan do¤umyapm›fl kad›nlar›n %53.3’ü bu hizmeti aile hekimlerinden,%89.0’u kad›n do¤um uzmanlar›ndan alm›flt›r. Gebelerin %74.0`üaile hekiminden, %94’ü kad›n do¤um uzman›ndan 14 hafta içindeilk DÖB’›n› alm›flt›r. Aile hekiminden DÖB alan do¤um yapm›flgebelerin %96’s›n›n kan bas›nc›, %92.5’inin a¤›rl›k ölçümü,%25.1’inin kalp oskültasyonu yap›lm›flt›r. Kad›n do¤um uzman›n-dan DÖB alan do¤um yapm›fl gebelerin %95.4’ünün kan bas›nc›,%91.8’inin a¤›rl›k ölçümü, %98.2’sinin ultrasonu, %90’›n›n kantetkiki yap›lm›fl; %31.5’ine aile planlamas› dan›flmanl›k hizmetleriverilmifltir. Sonuç: ‹stanbul’da gebelere say›sal olarak yeterli, ancak düflük ka-litede DÖB verilmifltir. Bu ba¤lamda; DÖB veren sa¤l›k persone-line düzenli aral›klarla hizmet içi e¤itimler verilmeli ve Sa¤l›k Ba-kanl›¤› izlem rehberinin daha aktif kullan›m› sa¤lanmal›d›r.

Anahtar sözcükler: Do¤um öncesi bak›m, aile hekimi, kad›n do-¤um uzman›, ‹stanbul

Correspondence: Binali Çatak, MD. Üsküdar Toplum Sa¤l›¤› Merkezi, Istanbul, Turkey.e-mail: [email protected]

Received: July 26, 2012; Accepted: December 29, 2012




Research Article


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Evaluation of prenatal care in Istanbul: a population based study

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IntroductionPrenatal care (PC) is the follow-up of mother and fetusregularly during entire pregnancy by well-educatedhealth personnel through required examinations andrecommendations. PC generally aims to make mothersto have a healthy pregnancy, to deliver healthy babiesand to protect health during pregnancy. Special pur-poses of PC are to detect diseases already existing inmother before pregnancy, to provide early diagnosisand treatment of diseases that may appear as a preg-nancy complication and to provide dispatch if needed,to determine risky pregnancy, to conduct intrauterinefollow-up of fetus, to make mother immune againsttetanus, to decide where, how and by who will deliverybe done, to inform mother about breast-feeding, gesta-tional hygiene, delivery, postnatal care, baby care andfamily planning methods after delivery.

The earlier prenatal care is initiated and performedregularly with high quality, the more maternal andfetal/infant deaths are decreased.[1] It was shown in theNational Maternal Death Study performed in 2005 thatthe death reasons of 61.6% of mothers who died werepreventable. It was pointed out in the same study thatPC is very essential since more than half of the motherswho died were late to define the problem, almost half ofthem were late to apply for health care, one fourth ofmothers did not receive PC, one fourth of mothers whoreceived PC got low quality service, also preeclampsiaand/or eclampsia was the second frequent reason formaternal death.[2] In this context, Health Ministry pre-pared and declared “Prenatal Care ManagementGuide” in order to provide high quality PC and stan-dardization in examinations of pregnants. In the guide,examination, measurement, test, and consultancy serv-ices which are required to be done and followed up 4times between weeks 18-24, 30-32 and 36-38 within 14weeks of each pregnancy were defined.[3]

In this study, it was aimed to evaluate PC servicesgiven by family physicians at primary care level and byobstetricians at secondary and tertiary care levels inIstanbul in terms of quantity and quality.

MethodApproximately 14 million of people live in Istanbulwhich is the biggest city of Turkey. It is the mosaic ofTurkey where all people migrating from every regionsof Anatolia live together. The city which is the eco-nomical artery of Turkey has 39 districts. In 2009, the

city had 54.4% of exportation and 55.9% of importa-tion of the whole country. In 2008, 43.1% of taxincome of Turkey was from Istanbul. While Gini coef-ficient of the city was 0.35, 8.3% of the city populationwas within first 20% zone and 43.5% was within thelast (fifth) 20% zone in terms of income level.[4]

During the period that the study was conducted,there were 3539 family physicians in Istanbul and therewere only 28 empty family physician positions.According to the Family Physician Information System(FPIS) (the population registered to FPIS was13,031,726), the average population per family physi-cian was 3682 at the same period while it was 3850based on Turkish Statistical Institute (TURKSTAT)(Istanbul population is 13,624,240 according toTURKSTAT).[5]

The study population of this cross sectional studycomposed of 99.254 women whose pregnancies wasrecorded by their family physicians (FP) on November27th, 2011 in Istanbul. According to TurkishPopulation Health Research, 4.3% of pregnants inIstanbul did not receive prenatal care. Accordingly, thesize of population representing the study in Epi Infoprogram was calculated as 1454, where prevalence was4%, margin of error was 1%, type 1 error level was 5%and confidence interval was 95%.

The population was arranged according to preg-nant numbers of districts and it was decided how manypregnants would be taken from each district. It wasplanned to choose each pregnant from a different fam-ily physician. Since total family physicians in Istanbulare more than the pregnants in the sample population,family physicians were chosen randomly first, and thenthe pregnants of those family physicians were chosenrandomly from FPIS.

The data of the study were collected by question-naire based on Prenatal Care Management Guide andTurkish Population and Health Research (TPHR).[3,6]

The questionnaire had questions including sociodemo-graphic and biodemographic data of women and serv-ices that should be given before prenatal care such asexamination, measurement, information and consul-tancy. After required permissions are received, datawere collected in between January 2nd and 16th, 2012via face-to-face interviews by obstetricians and nursesworking in public health centers (PHC) in Istanbulafter receiving verbal informed consent from preg-nants. Before collecting data, obstetricians and nurseswho will participate into these interviews were trained

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for 4 hours about the purpose of the study and the aimsof each question in order to provide standardization incollecting data. The preliminary test of questionnairewas done on 13 pregnants who were not included intothe study and required modifications were done in thequestionnaire. One obstetrician or nurse from eachPHC was assigned for completing missed areas of col-lected questionnaire and to get an appointment and tomake the interview with pregnants who were working.Questionnaire forms of 53 pregnants were answered byphone interview.

Among 1454 pregnants chosen for the study, 94%of them (1368 pregnants) were reached. Among thosewho could not be reached, 63 of them could not be

found in the given address and 24 of them refused toparticipate to the study. Data were analyzed by SPSS10.5 software. Frequency, percentage, central clustercriteria (mean and median) and central prevalence cri-teria (standard deviation, maximum and minimum val-ues) were used in the analyses as definitive criteria.

ResultsSome sociodemographic data of pregnants are summa-rized in Table 1. While 32.9% of pregnants were bornin Marmara Region, 35.2% of pregnants’ fathers wereborn in the Black Sea Region. While 9.5% of womenwere uneducated, only 2.9% of their spouses were une-

Table 1. Sociodemographic data of the pregnants (Istanbul, 2011).

Sociodemographic Data n (%) Sociodemographic Data n (%)

Birth place of woman* Family type†

Marmara Region 449 (32.9) Extended family 359 (26.2)

Black Sea Region 321 (23.5) Nuclear family 1007 (73.8)

Eastern Anatolia Region 229 (16.8) Household size||

Central Anatolia Region 142 (10.4) 4 and below 1034 (75.8)

Southeastern Anatolia Region 119 (8.7) 5 and above 330 (24.2)

Mediterranean Region 46 (3.4) Marriage method||

Aegean Region 35 (2.6) Arranged 602 (44.1)

Abroad 24 (1.8) Companionate 762 (55.9)

Birth place of woman’s father† Kinship to spouse‡

Marmara Region 124 (9.1) Available 236 (17.3)

Black Sea Region 481 (35.2) N/A 1129 (87.2)

Eastern Anatolia Region 315 (23.1) Civil marriage||

Southeastern Anatolia Region 149 (10.4) Available 1329 (97.4)

Central Anatolia Region 202 (14.8) N/A 35 (2.6)

Mediterranean Region 39 (2.9) Health coverage*

Aegean Region 29 (2.1) N/A 116 (8.5)

Abroad 27 (2.0) Green health card 34 (2.5)

Educational background of woman‡ Social security institution 1215 (89.0)

Uneducated 130 (9.5) Employment of woman*

Primary School 454 (33.2) Unemployed 1077 (78.7)

Secondary School 230 (16.8) Wage-earning employment 288 (21.3)

High School 315 (23.0) Employment of spouse¶

University 233 (17.0) Unemployed / temporary jobs 181 (13.2)

Educational background of spouse§ Public sector 105 (7.7)

Uneducated 39 (2.9) Private sector 810 (59.2)

Primary School 440 (32.2) Self-employed 163 (19.2)

Secondary School 247 (18.1) Total income of family‡

High School 339 (24.8) Sufficient subsistence 386 (28.4)

University 296 (21.6) Barely subsistence 708 (52.0)

Total 1368 (100.0) Not sufficient 267 (19.6)

Total 1368 (100.0)

*Missing data of 3 people, †missing data of 2 people, ‡missing data of 6 people, §missing data of 7 people, ||missing data of 4 people, ¶spouses whowere doing their military services were excluded.



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ducated; 26.2% of them were living in extended fami-lies and 24.2% of them were living in a family consist-ing of 5 or more people. More than half of the preg-nants (55.9%) were married through an arranged mar-riage, 17.3% of them were relative to their spouses;while 2.6% of them had no civil marriage, 8.5% ofthem had no health insurance. Totally 78.7% ofwomen were not working in a wage-earning job and13.2% of their spouses were either unemployed orworking in a temporary job. It was stated by 19.6% ofwomen that total income of family was not sufficient.In the study, the ages of 3.1% of women were 19 orbelow while 10.5% of them were 35 and above. Thepregnancy was not desired by 3.5% of women and2.9% of their spouses. Current pregnancy was the firstpregnancy of 34.6% of women. The percentage ofwomen who had four or more pregnancies was 16.6%.Among those who had at least one pregnancy exceptthe current pregnancy, 28.9% of women had sponta-

neous abortion, 10.9% of them had intentional abor-tion and 4.5% of them had stillbirth. The rate of childdeath below 5 y/o was 3%. Almost the half of women(49.3%) had one living child. While 52.9% of womenhad their previous deliveries at a private hospital, only4.6% of them delivered at home (Table 2).

The rate of smoking is 16.0% for pregnants and49.2% for their spouses, and 29.7% of pregnants arepassive smokers. It was found that 82.5% of the preg-nants were using iron preparations (not given in thetable). The distribution of PC from family physiciansand obstetricians received by pregnants according togestational week can be seen in Table 3. During theperiod when the study was conducted, 10.9% of preg-nants who were within 14 gestational weeks and 12.3%of pregnants who previously delivered did not receivePC from their family physicians. When PC servicereceived from obstetrician is evaluated according to ges-tational week, 1.3% of pregnants who were within 14

Table 2. Biodemographic data of the pregnants (‹stanbul, 2011).

Biodemographic data n (%) Biodemographic data n (%)

Age of woman* In pregnants who delivered at least once;

19 and below 43 (3.1) Spontaneous abortion

20–24 311 (22.8) Yes 259 (28.9)

25–29 500 (36.6) No 636 (71.1)

30–34 369 (27.0) Intentionally abortion

35 and above 144 (10.5) Yes 98 (10.9)

Desiring pregnancy by woman† No 797 (89.1)

Desired 1159 (85.0) Stillbirth

Desired later 157 (11.5) Yes 40 (4.5)

Never desired 48 (3.5) No 855 (95.5)

Desiring pregnancy by spouse‡ Child death below 5 y/o

Desired 1201 (88.2) Yes 27 (3.0)

Desired later 122 (8.9) No 868 (97.0)

Never desired 40 (2.9) Living children

Total pregnancy 0 90 (10.1)

1st pregnancy 473 (34.6) 1 441 (49.3)

2nd pregnancy 383 (28.0) 2 267 (29.8)

3rd pregnancy 285 (20.8) 3 and more 97 (10.8)

4th and more 227 (16.6) Where previous pregnancy was ended

Total 1368 (100.0) Private hospital 467 (52.9)

Public hospital 348 (39.4)

University 15 (1.7)

Home birth 41 (4.6)

Delivery on the way 12 (1.4)

Total 895 (100.0)

*Missing data of 1 person, †missing data of 3 people, ‡missing data of 5 people

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gestational weeks and 3.5% of pregnants who previous-ly delivered did not receive PC from their obstetricians.

In Table 4, the distribution of the services of exam-ination, measurement and consultancy according togestational weeks during PC have been summarized.During the period when the study was conducted, all ofthe pregnants who were within 14 gestational weeksgot their first gestational examination by their familyphysicians. First gestational examination of 57.1% ofpregnants who delivered previously was done within 14weeks. Weights of 92.5% and blood pressure of 96.0%of pregnants delivered previously were measured, andblood analysis of 61.3% of these women and urineanalysis of 47.2% of these women were carried out.

In Table 5, PC services received from obstetriciansby pregnants have been summarized. While all thepregnants below 14 gestational weeks received PC ator before 14 weeks, 90.9% of women who deliveredreceived their first PC service at or before 14 weeks.Height measurement of 36.5%, blood pressure meas-urement of 95.4%, and ultrasonography of 98.2%women who delivered were carried out and 37.1% ofthem were informed about breast-feeding.

DiscussionIt is hard to say that field studies regarding PC servic-es have been sufficiently performed during the last fiveyears especially in Istanbul. Therefore, it is consideredessential to carry out this study in Istanbul in terms ofestablishing a reference point for field studies to beperformed in the future.

In this study, it was aimed to evaluate PC servicesgiven by family physicians at primary care level and byobstetricians at secondary and tertiary care levels inIstanbul in terms of quantity and quality. FamilyPractice Regulation obliges all family physicians toprovide PC service during pregnancy for every preg-nant registered to regarding family physician.[7]

Prenatal Care Management Guide has defined PC tobe given by family physician in terms of quality andquantity. According to the guide, family physicians arerequired to provide PC at least once for all pregnantsbelow 25 weeks, at least twice for all pregnants below33 weeks, and at least four times for all women whodelivered their babies.[3]

According to the study, 6% of pregnants below 25weeks received no PC while 33.5% of them received

Table 3. Distribution of prenatal care (PC) from family physicians and obstetricians received by pregnants according to gestationalweek (Istanbul, 2011).

14< 15–24 25–32 33≥ Deliveredn (%)* n (%)* n (%)* n (%)* n (%)*

Family physician

0 26 (10.9) 21 (6.0) 24 (7.1) 9 (3.5) 28 (12.3)

1 110 (57.0) 117 (33.5) 44 (13.1) 21 (8.1) 17 (7.5)

2 34 (17.6) 112 (32.1) 93 (27.7) 35 (13.6) 26 (11,5)

3 16 (8.3) 58 (16.6) 72 (21.4) 61 (23.6) 35 (15.4)

4> 12 (6.2) 41 (11.7) 103 (30.7) 132 (51.2) 121 (53,3)

Mean 1.5 (±1.5) 2.0 (±1.4) 3.0 (±2.0) 3.9 (±2.2) 3.9 (±2.9)

Median 1 (0–11) 2 (0-10) 3 (0-13) 4 (0-15) 4 (0-20)

Obstetrician†

0 3 (1.5) 6 (1.7) 4 (1.2) 2 (0.8) 8 (3.5)

1 43 (21.7) 19 (5.4) 10 (3.0) 4 (1.6) 3 (1.3)

2 37 (18.7) 29 (8.3) 15 (4.5) 7 (2.7) 7 (3.1)

3 47 (23.7) 50 (14.3) 29 (8.6) 13 (5.0) 7 (3.1)

4> 68 (34.3) 245 (70.2) 277 (82.4) 232 (89.9) 202 (89.0)

Mean 3.3 (±2.3) 5.0 (±3.2) 6.4 (±3.2) 7.8 (±3.5) 8.3 (±4.1)

Median 3 (0-15) 4 (0-30) 6 (0-20) 8 (0-20) 9 (0-20)

Total 198 (100.0) 349 (100.0) 336 (100.0) 258 (100.0) 227 (100.0)

*Column percentage, †missing data of 3 people

PC number

Gestational weeks



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once; 47.9% of pregnants below 33 weeks received PCtwice or less and 46.7% of women who delivered theirbabies received PC less than four times. In a field studyconducted in Karabük city center, 23.7% of pregnants

below 25 weeks received PC once, 14% of pregnantsbelow 33 weeks received PC twice or less and 33.3% ofwomen who delivered their babies received PC lessthan four times from their family physicians.[8]

Table 4. Distribution of examination, measurement and consultancy services according to gestational week received during PC fromfamily physicians by pregnants (Istanbul, 2011).

Gestational weeks

14< 15–24 25–32 33≥ Deliveredn (%)* n (%)* n (%)* n (%)* n (%)*

First PC time

At 14 weeks and below 172 (100.0) 278 (85.0) 199 (64.2) 153 (62.2) 113 (57.1)

At 15 weeks and above - 49 (15.0) 111 (35.8) 93 (37.8) 85 (42.9)

Height measurement

Measured 71 (41.3) 112 (34.1) 121 (38.8) 87 (34.9) 78 (39.2)

Not measured 101 (58.7) 216 (65.9) 191 (61.2) 162 (65.1) 121 (60.8)

Weight measurement

Measured 148 (86.0) 229 (91.2) 288 (92.3) 238 (95.6) 184 (92.5)

Not measured 24 (14.0) 29 (8.8) 24 (7.7) 11 (4.4) 15 (7.5)

Blood pressure measurement

Measured 150 (87.2) 302 (92.1) 299 (95.8) 241 (96.8) 191 (96.0)

Not measured 22 (12.8) 26 (7.9) 13 (4.2) 8 (3.2) 8 (4.0)

Heart auscultation

Done 40 (23.3) 66 (20.1) 91 (29.2) 68 (27.3) 50 (25.1)

Not done 132 (76.7) 262 (79.9) 221 (70.8) 181 (72.7) 149 (74.9)

Children heart beat

Listened 26 (15.1) 132 (40.2) 226 (72.4) 205 (82.3) 162 (81.4)

Not listened 146 (84.9) 196 (59.8) 86 (27.6) 44 (17.7) 37 (18.6)

Blood analysis

Done 116 (67.4) 173 (52.7) 203 (65.1) 158 (63.5) 122 (61.3)

Not done 56 (32.6) 155 (47.3) 109 (34.9) 91 (36.5) 77 (38.7)

Urine analysis

Done 59 (34.3) 123 (7.5) 136 (43.6) 118 (47.4) 94 (47.2)

Not done 113 (65.7) 205 (62.5) 176 (56.4) 131 (52.6) 105 (52.8)

Breast-feeding information

Given 25 (14.5) 43 (13.1) 70 (22.4) 88 (35.3) 97 (48.7)

Not given 147 (85.5) 285 (86.9) 242 (77.6) 161 (64.7) 102 (51.3)

Family planning information

Given 25 (14.5) 43 (13.1) 52 (16.7) 64 (25.7) 71 (35.7)

Not given 147 (85.5) 285 (86.9) 260 (83.3) 185 (74.3) 128 (64.3)

Information about complaints that may be seen during pregnancy

Given 71 (41.3) 134 (40.9) 138 (44.2) 112 (45.0) 100 (50.3)

Not given 101 (58.7) 194 (59.1) 174 (55.8) 137 (55.0) 99 (49.7)

Planning delivery location

Done 41 (23.8) 65 (19.8) 94 (30.1) 107 (43.0) 102 (51.3)

Not done 131 (76.2) 263 (80.2) 218 (69.9) 142 (57.0) 97 (48.7)

Total 172 (100.0) 328 (100.0) 312 (100.0) 249 (100.0) 199 (100.0)

*Column percentage

Parameter

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In the study, mean follow-up number per pregnantwho delivered is 3.9. In brief, PC service provided byfamily physicians in Istanbul according to gestationalweek is below the desired level in quantity. However,

when it is considered that mean follow-up number perpregnant at primary care level in Istanbul is 2 accord-ing to 2010 Health Statistics Annual,[9] it can be saidthat there is almost 100% increase in the number of

Table 5. Distribution of examination, measurement and consultancy services according to gestational week received during PC fromobstetricians by pregnants (Istanbul, 2011).

Gestational weeks

14< 15–24 25–32 33≥ Deliveredn (%)* n (%)* n (%)* n (%)* n (%)*

First PC time

14 hafta ve alt›At 14 weeks and below 195 (100.0) 329 (95.9) 308 (92.8) 233 (91.0) 199 (90.9)

At 15 weeks and above - 14 (4.1) 24 (7.2) 23 (9.0) 20 (9.1)

Height measurement

Measured 54 (27.7) 93 (27.1) 100 (30.1) 66 (25.8) 80 (36.5)

Not measured 141 (72.3) 250 (72.9) 232 (69.9) 190 (74.2) 139 (63.5)

Weight measurement

Measured 134 (68.7) 285 (83.1) 282 (84.9) 224 (87.5) 201 (91.8)

Not measured 61 (31.3) 58 (16.9) 50 (15.1) 32 (12.5) 18 (8.2)

Blood pressure measurement

Measured 124 (63.6) 279 (81.3) 289 (87.0) 232 (90.6) 209 (95.4)

Not measured 71 (36.4) 64 (18.7) 43 (13.0) 24 (9.4) 10 (4.6)

Heart auscultation

Done 55 (28.2) 102 (29.7) 109 (32.8) 87 (34.0) 91 (41.6)

Not done 140 (71.8) 241 (70.3) 223 (67.2) 169 (66.0) 128 (58.4)

Ultrasonography

Done 184 (94.4) 336 (98.0) 325 (97.9) 250 (97.7) 215 (98.2)

Not done 11 (5.6) 7 (2.0) 7 (2.1) 6 (2.3) 4 (1.8)

Blood analysis

Done 142 (72.8) 277 (80.8) 293 (88.3) 228 (89.1) 197 (90.0)

Not done 53 (27.2) 66 (19.2) 39 (11.7) 28 (10.9) 22 (10.0)

Urine analysis

Done 131 (67.2) 256 (74.6) 281 (84.6) 218 (85.2) 193 (88.1)

Not done 64 (32.8) 87 (25.4) 51 (15.4) 38 (14.8) 26 (11.9)

Breast-feeding information

Given 14 (7.2) 38 (11.1) 44 (13.3) 37 (14.5) 83 (37.9)

Not given 181 (92.8) 305 (88.9) 288 (86.7) 219 (85.5) 136 (62.1)

Family planning information

Given 11 (5.6) 26 (7.6) 32 (9.6) 29 (11.3) 69 (31.5)

Not given 184 (94.4) 317 (92.4) 300 (90.4) 227 (88.7) 150 (68.5)

Information about complaints that may be seen during pregnancy

Given 107 (54.9) 201 (58.6) 210 (63.3) 159 (62.1) 152 (69.4)

Not given 88 (45.1) 142 (41.4) 122 (36.7) 97 (37.9) 67 (30.6)

Planning delivery location

Done 67 (34.4) 120 (35.0) 163 (49.1) 144 (56.3) 131 (59.8)

Not done 128 (65.6) 223 (65.0) 169 (50.9) 112 (43.8) 88 (40.2)

Total 195 (100.0) 343 (100.0) 332 (100.0) 256 (100.0) 219 (100.0)

*Column percentage

Parameter



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follow-up per pregnant in 2011. The possible reasonfor this increase is the increasing number of physiciansin Istanbul when family medicine was put into practicein Istanbul in 2011. According to the data of IstanbulHealth Administration, while there were 2007 physi-cians working in health centers on October 31st, 2010,there were 3539 family physicians during the periodwhen the study was carried out.

All of the women except 1.7% of them got exam-ined by an obstetrician in the study. While 89% ofwomen who delivered received PC for four or moretimes, mean PC per pregnant was found as 8.3. Dataregarding PC in Turkish Population and HealthResearch (TPHR) was evaluated according to the mostqualified health personnel giving this service. When itis considered that pregnancy ultrasonography is per-formed by obstetricians, 96.2% of pregnants receivingPC were examined ultrasonographically; in otherwords, 96.2% of pregnants receiving PC were exam-ined by an obstetrician and 73.4% of them received PCfor four or more times.[6] In a study performed inAd›yaman, 93.4% of pregnants were examined by anobstetrician at least once, and mean examination perpregnant was reported as 4.4%.[10]

Both in this study, and TPHR and other studiesshow that pregnants received sufficient number of PCfrom obstetricians. In PC Management Guide, it isstated that pregnancy should be detected until 14weeks at the latest, and first PC should be given with-in this period.[3] In the study, approximately 5 of each15 pregnants who delivered their babies received theirfirst PC within 14 weeks. In the study performed inKarabük city center, 7 of each 10 pregnants who deliv-ered their babies received their first PC within first 14weeks.[8] In TPHR 2008, approximately 7 of each 10pregnants received their first PC within 3 months.[6]

Consequently, when considered according to gesta-tional week, determining pregnancy within 14 weeksby family physicians in Istanbul is below the desiredlevel. This is probably caused by two reasons. The firstreason is that health personnel working at primary carelevel in Istanbul are not aware of the significance ofproviding PC early and the second reason is that dis-patch system is not applied properly. As a result, preg-nants prefer obstetricians for pregnancy examinationsrather than family physician. This preference is clearlyunderstood that more than 90% of pregnants whodelivered received their PC within 14 weeks from anobstetrician.

Physical examination, test and consultancy servicesthat should be given to pregnants have been defined inthe PC Management Guide. Except height measure-ment, the Guide requires all parameters asked in thequestionnaire to be done in each PC.[3] In the study, thelevel of providing parameters defined in the Table 4 topregnants by family physicians and family health per-sonnel increases as gestational week increases. Whilemeasurements of weight and tension of pregnantamong these parameters are above 90%, other param-eters are at quite low level. Similar findings wereobtained in field studies carried out in Karabük andAd›yaman[8,10] The findings are same for the sameparameters in terms of obstetricians. On the otherhand, when compared to TPHR 2008 data whereblood pressure, weight measurement, blood and urineanalyses and USG are evaluated, the level of providingthese services in Istanbul is above the country aver-age.[6]

In brief, it is hard to say that PC provided inIstanbul by family physicians and obstetricians is in suf-ficient quality. The possible reasons are that familyphysicians and obstetricians do not have sufficient levelof knowledge about the content of PC ManagementGuide and that both physician groups do not aware thesignificance of PC even they have sufficient level ofknowledge about PC.

ConclusionConsequently, PC provided by family physicians andobstetricians are not at a sufficient level in terms ofgestational week and performing first examinationwithin 14 weeks, although PC service per pregnant atprimary care level in Istanbul is increased almost 100%compared to year 2010. On the other hand, pregnantsreceived sufficient level of PC at secondary and tertiarycare levels. When PC provided both in primary andsecondary care levels are evaluated together, 99.6% ofpregnants received PC. Within this context, it can besaid that the target of providing PC at least once to98% of all pregnants in the country.[11] in terms of“2005-2015 National Strategic Action Plan Sexual andReproductive Health” has been achieved. However,PC provided to pregnants in primary, secondary andtertiary care levels are not in sufficient quality. Whilehealth personnel providing PC gave priority to physi-cal examination and laboratory analyses, consultancyand information services were insufficient.

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Within this context; 1. Studies evaluating knowledge, attitude and behav-

iors of health personnel about PC ManagementGuide providing PC service at every level should beconducted.

2. In accordance with the conclusions of these studies,required trainings should be provided periodically.

3. Studies determining the effects of trainings given tohealth personnel of public health centers should beconducted; conclusions should be evaluated and ifrequired, current PC policy should be revised locally.The study was carried out over pregnants registered

to family physicians. The possibility of the existence ofpregnants not registered to family physicians is themost essential limitation of the study.


References1. Ak›n A. Türkiye’de ana sa¤l›¤›, aile planlamas› hizmetleri ve

isteyerek düflükler. In: Ak›n A, editor. 1998 Türkiye Nüfusve Sa¤l›k Araflt›rmas› ‹leri Analiz Sonuçlar›. Ankara:Hacettepe Üniversitesi Hastaneleri Bas›mevi; 2002. p. 151-82.

2. Hacettepe Üniversitesi Nüfus Etütleri Enstitüsü, ICON-INSTITUT Public Sector Gmbh ve BNB Dan›flmanl›kSa¤l›k Bakanl›¤› Ana Çocuk Sa¤l›¤› ve Aile Planlamas› GenelMüdürlü¤ü ve Avrupa Komisyonu Türkiye Delegasyonu.

Türkiye Ulusal Anne Ölümleri Çal›flmas›. Ankara:Hacettepe Üniversitesi; 2005. p. 51-88.

3. Sa¤l›k Bakanl›¤› Ana Çocuk Sa¤l›¤› Aile Planlamas› GenelMüdürlü¤ü. Do¤um öncesi bak›m yönetim rehberi. Ankara:Sa¤l›k Bakanl›¤›; 2009.

4. Türkiye ‹statistik Kurumu. Türkiye istatistik y›ll›¤›. Ankara:Türkiye ‹statistik Kurumu; 2011.

5. Türkiye ‹statistik Kurumu. Göç ‹statistikleri.www.tuik.gov.tr/VeriBilgi.do?tb_id=38&ust_id=1102 Nisan2002.

6. Hacettepe Üniversitesi Nüfus Etütleri Enstitüsü, Sa¤l›kBakanl›¤› Ana Çocuk Sa¤l›¤› ve Aile Planlamas› GenelMüdürlü¤ü, Baflbakanl›k Devlet Planlama Teflkilat›Müsteflarl›¤› ve TÜB‹TAK. Türkiye Nüfus ve Sa¤l›kAraflt›rmas›, 2008. Ankara: Hacettepe Üniversitesi; 2009. p.149-69.

7. Sa¤l›k Bakanl›¤›. Aile Hekimli¤i Uygulama Yönetmeli¤i.http://www.saglik.gov.tr/TR/belge/1-0376/aile-hekimligi-uygulama-yonetmeligi.html17 Ocak 2011

8. Çatak B, Davas A, Zencir M. Karabük Toplum Sa¤l›¤›Merkezi bölgesinde do¤um öncesi bak›m hizmetlerinin nice-lik ve niteli¤i. TAF Preventive Medicine Bulletin2012;11:153-62.

9. Sa¤l›k Bakanl›¤›. Sa¤l›k istatistikleri y›ll›¤› 2010. Ankara:Sa¤l›k Bakanl›¤›; 2011. p. 49-50.

10. Çatak B. Ad›yaman 2 No’lu Toplum Sa¤l›¤› MerkeziBölgesinde 2007 y›l›nda canl› do¤um yapan kad›nlar›ndo¤um öncesi, do¤um ve do¤um sonras› izlemleri.12. UlusalHalk Sa¤l›¤› Kongresi Özet Kitab›, Ankara, 21-25 Ekim2008.

11. Sa¤l›k Bakanl›¤›. Sa¤l›k sektörü için Ulusal Stratejik EylemPlan›. http://sbu.saglik.gov.tr/tusp/turkce/yayinlar/pdf_dokumanlar/01_USEP.pdf

Retrospective analysis of stillbirth cases in a regional hospital

Muhammet Erdal Sak1, Mehmet S›dd›k Evsen1, Hatice Ender Soydinç1, Sibel Sak2, Serdar Baflarano¤lu1, Ahmet Yal›nkaya1

1Department of Obstetrics and Gynecology, Faculty of Medicine, Dicle University, Diyarbak›r, Turkey2Gynecology and Obstetrics Clinic, Diyarbak›r Obstetrics and Pediatrics Hospital, Diyarbak›r, Turkey

Introduction

Fetal stillbirth is the state of a newborn after 20 weeksgestation or at and above 500 g of birth weight display-ing no vitality indication during after delivery.[1]

Reasons of newborn death can be associated with fetal,placental and maternal issues. Fetal stillbirth has been

reported as 5/1000. Many reasons such as black race,increased maternal age, obesity, smoking, previousstillbirth history, fetal growth restriction, multiplepregnancy and maternal diseases are risk factors forstillbirth. It has been reported that fetal stillbirth rate isreduced in time by increased prenatal diagnostic meth-

Abstract

Objective: To evaluate the stillbirth cases and to determine therisk factors for our region. Methods: Maternal age, parity, gestational weeks before birth,vaginal and cesarean delivery rates, indications of cesarean section,detected fetal anomalies and maternal diseases of 308 cases withdiagnosed intra-uterine fetal death were evaluated and comparedwith randomly selected 300 live births in our clinic.Results: In a five-year period, stillbirth rate was 2.02% in 15,203deliveries. Mean age was 30.6±7.2, prepartum gestational week was30, 5±5.3 and mean parity was 3.6±3.1 in stillbirths. Pregnancy-induced hypertensive disorders (19.4%), fetal abnormality rate(12.9%), and gestational diabetes (2.2%) were significantly high instillbirths (p<0.001).Conclusion: In our study, the most common causes of stillbirthswere pregnancy-induced hypertensive disorders, fetal anomaliesand gestational diabetes. Increasing the protective and preventivehealth care in primary and secondary antenatal care centers, andtimely treatment for high-risk pregnancies may contribute to thereduction of the rate of stillbirths.

Key words: Stillbirth, antenatal care.

Bir bölge hastanesinde ölü do¤um olgular›n›nretrospektif analiziAmaç: Ölü do¤um yapan olgular›n de¤erlendirilmesi, risk faktör-lerinin bölgemiz için belirlenmesi.Yöntem: Klini¤imizde intrauterin fetal ölüm tan›s› konup do¤u-mu gerçekleflen 308 olgu anne yafl›, paritesi, do¤um öncesi gestas-yonel hafta, vajinal ve sezaryen do¤um oranlar›, sezaryen endikas-yonlar›, tespit edilen fetal anomaliler, maternal hastal›klar yönün-den de¤erlendirildi ve random olarak seçilen 300 canl› do¤umlakarfl›laflt›r›ld›.Bulgular: Befl y›ll›k sürede 15.203 do¤umdan, ölü do¤um oran›%2.02 olarak saptand›. Ölü do¤umlar›n yafl ortalamas› 30.6±7.2,prepartum gebelik haftas› 30.5±5.3 ve paritesi 3.6±3.1 olarak bu-lundu. Gebeli¤in indükledi¤i hipertansif hastal›klar (%19.4), fetalanomali oran› (%12.9) ve gestasyonel diyabet (%2.2) ölü do¤um-larda anlaml› flekilde yüksek idi (p<0.001). Sonuç: Çal›flmam›zda ölü do¤umlar›n en s›k görülen sebepleri ge-beli¤in indükledi¤i hipertansif hastal›klar, fetal anomaliler ve ges-tasyonel diyabet olarak tespit edildi. Antenatal bak›m›n yap›labil-di¤i primer ve sekonder merkezlerde koruyucu ve önleyici sa¤l›khizmetlerinin artt›r›lmas›, yüksek riskli gebeliklerin zaman›nda te-davisiyle ölü do¤um oran›n›n azalt›lmas›na katk› sa¤lanabilir. Anahtar sözcükler: Ölü do¤um, antenatal bak›m.

Correspondence: Muhammet Erdal Sak, MD. Dicle Üniversitesi T›p FakültesiKad›n Hastal›klar› ve Do¤um Anabilim Dal›, Diyarbak›r, Turkey.e-mail: [email protected]

Received: October 18, 2012; Accepted: November 14, 2012




Research Article


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ods, early abortion of fetuses with anomaly andimproved antenatal care.[2]

In this study, we aimed to evaluate cases retrospec-tively who gave labor in our clinic after intrauterinefetal stillbirth in terms of maternal age, parity, gesta-tional week, delivery type, cesarean indications, detect-ed fetal anomalies and maternal diseases.

MethodOf totally 15,203 deliveries carried out in theObstetrics and Gynecology Department of MedicalSchool of Dicle University within 5 years from May2006 to 2011, 308 stillbirth cases were evaluated retro-spectively. Data were obtained from digital records ofhospital automation system, birth records and patientfiles.

Totally 308 stillbirth cases (Group 1) and 300 livebirth cases (Group 2) were included into the study.Both groups were evaluated in terms of maternal age,gravida, parity, gestational week, hypertensive diseasesseen during pregnancy, delivery type, cesarean indica-tions, birth weights, and fetal anomalies. Gestationalage was determined by last menstrual period and/or

ultrasonographic evaluation of fetal biometric parame-ters. Fetal stillbirth was diagnosed by establishing non-existence of fetal cardiac pulse via ultrasonography(Voluson 730 Pro, General Electric, Vienna, Austria).Fetal anomalies were found by prepartum ultrasonog-raphy and diagnoses of postnatal physical examinationof fetus. Gestational diabetes diagnosis was establishedby 100 gram oral glucose tolerance test. Statisticalanalysis of data was done by SPSS (Statistical Packagefor Social Science, SPSS Inc., Chicago, IL, USA) version15.0. Chi-square and Mann-Whitney U test wereapplied for both groups. P<0.005 was considered asstatistically significant.

ResultsTotally 308 stillbirth cases were found in 15,203 deliv-eries in five years at Obstetrics and GynecologyDepartment of Medical School of Dicle University.During this period, stillbirth rate was found as 2.02%.Demographic data of patients who had stillbirth(Group 1) and control group patients (Group 2) areshown in Table 1. No significant difference wasobserved between two groups in terms of mean age(p>0.05).

Table 2. Hypertensive diseases, fetal anomaly, gestational diabetes and cesarean delivery rates.

Group 1 Group 2 p

Gestational hypertensive diseases 19.4% 9.0% <0.001

Fetal anomaly 12.9% 2.0% <0.001

Gestational diabetes 2.2% 0.6% <0,05

Cesarean rates 41.2% 58.8% <0.001

Table 1. Demographic data of patients in Group 1 and ve Group 2.

Group 1 Group 2 (mean ± SD) (mean ± SD) p

Age 30.6±7.2 29.9±7.0 >0.05

Gravida 5.2±3.5 3.7±3.0 <0.001

Parite 3.6±3.1 2.4±2.8 <0.001

Abort 0.62±1.1 0.31±0.8 <0.001

Live 3.6±3.2 2.4±2.8 <0.001

Gestational week 30.5±5.3 34.1±5.4 <0.05

Newborn weight (gram) 1685.4±991.8 2179.7±1023.3 <0.001



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Pregnancy, abortus and living child number inintrauterine fetal death cases were observed statisticalsignificant compared to control group (p<0.001).Hypertensive diseases, deliveries with fetal anomalyand gestational diabetes were significantly high in thecases of Group 1 while cesarean numbers were signifi-cantly high in Group 2 (Table 2). Hypertensive dis-eases were 19.48% and 9% in Group 1 and Group 2cases, respectively (p<0.001).

Fetal anomaly frequency was 13% in patient groupand 2% in Group 2 cases (p<0.001) and it was statisti-cally significant. Most frequently observed fetal anom-

alies in Group 1 cases were hydrocephaly and anen-cephaly, respectively (Table 3).

Cesarean rate was higher in Group 2 cases(p<0.001). The most frequent cesarean indications inGroup 1 cases were previous cesarean underwent, abla-tio placenta, dystocia and uterus rupture (Table 4).

DiscussionFetal stillbirth is the state of a newborn after 20 weeksgestation or at and above 500 g of birth weight display-ing no vitality indication during after delivery.[1] Fetaldeaths may be associated with maternal, placental and

Table 3. Fetal anomalies and their rates seen in Group 1 cases.

Fetal anomalies n %

Hydrocephaly 9 22.5

Anencephaly 7 17.5

Immune hydrops 6 15

Non-immune hydrops 4 10

Hydrocephaly and meningomyelocele 3 7.5

Cleft palate-lip 2 5

Gastroschisis 2 5

Anencephaly and spina bifida 2 5

Omphalocele and spina bifida 2 5

Hydrocephaly ve hand-foot deformity 2 5

Hydrocephaly and spina bifida-pes equinovarus 1 2.5

Single umbilical artery 1 2.5

Table 4. Cesarean indications of Group 1.

Cesarean indications n %

Previous cesarean history 26 30.9

Ablatio placenta 25 29.7

Dystocia 9 10.7

Uterus rupture 9 10.7

Macrosomia 8 9.6

Placenta previa totalis 2 2.4

Foot presentation 1 1.2

Breech presentation 1 1.2

Transverse presentation 1 1.2

HELLP 1 1.2

Severe preeclampsia 1 1.2

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fetal reasons.[3] In our study, stillbirth rate was found as2.02% which is higher than those reported in the liter-ature. The reason for high rate can be explained byconsidering that our hospital is a reference center forSoutheastern Anatolia region. For maternal factors,Fretts et al. reported that advanced maternal age is arisk factor independent from stillbirth history.[4] Lunaet al. stated that maternal age is not a risk factor.[5] Inour study, there was no significant difference betweenmean maternal age and the group having live birth.

In a study performed by Öndero¤lu et al., it wasreported that 326 of 513 pregnants who had stillbirthwere multipara and gestational week was significantlylower in the stillbirth group than those having livebirth.[6] In our study, gestational week was lower instillbirth group. Losing fetus at early weeks due to fetalanomalies, pregnancy-induced hypertensive diseases,and complications related with gestational diabetesmay explain this outcome.

Kale et al. conducted a ten-year retrospective studyin 2005 and they found significant difference betweennewborn weights.[7] In our study, significantly low new-born weights in stillbirths may be interpreted that fetusis lost at early weeks due to accompanying anomaliesand diseases and therefore birth weight is low.Increased body mass index (BMI) and smoking increas-es the risk in terms of stillbirth. Carbohydrate intoler-ance increases stillbirth risk in gestational diabeticpatients.[8,9] In our study, gestational diabetes cases weresignificantly high in stillbirth group compared to con-trol group.

Congenital anomalies among fetal causes are signif-icant when evaluating stillbirth etiology. Faye-Peterson et al. reported that one third of stillbirths iscaused by fetal structural anomalies and among them,neural tube defects (NTD), hydrops, isolated hydro-cephaly and complex congenital cardiac diseases werethe frequent ones.[10] In the study performed by Pauliand Reiser, it was reported that the most of the still-births due to fetal reasons had a major malformationthat may cause a fetal death.[11] On the contrary,Copper et al. found in their work that malformations(prenatally) without fetal autopsy information was only5.6%.[12] In the study performed by Kale et al., fetalanomaly rate was found as 12.12%. This rate is consis-tent with the rate (12.99%) that we found in ourstudy.[7] In our study, neural tube defects were the mostfrequently observed structural anomalies (55%).Madazl› et al. reported anencephaly as the most fre-

quent anomaly type among NTD.[13] In our study,hydrocephaly was the most frequent fetal anomaly.

Gürel et al. examined 51 stillbirth cases in theirstudies and they reported hypertensive diseases(preeclampsia-eclampsia) as the most frequent rea-son.[14] Hypertensive diseases associated with pregnan-cy was found as the most frequent reason in stillbirthetiology. Stillbirth due to ablatio placenta is 14%.Totally 50% of these cases develop pregnancy-inducedhypertension.[4] In our study, cesarean rate is lower inthe stillbirth cases compared to the control groupwhile the ablatio placenta is among the most frequentcesarean indication reasons.

ConclusionConsequently, pregnancy-induced hypertensive dis-eases, fetal anomalies and gestational diabetes werefound as the most frequent reasons for stillbirths in ourstudy. As our center is the reference hospital in theregion, stillbirth rates in our study are higher thannational average and those reported in the literature.Also patients in our region do not visit our center forantenatal follow-up; when such problems are resolved,stillbirth rate will be decreased in our region.Increasing protective and preventive healthcare servic-es in primary and secondary center where antenatalcare is available, and timely treatment of high-riskpregnancies may contribute to decrease stillbirth rate.


References

1. MacDorman MF, Kirmeyer S. Fetal and perinatal mortality.United States. 2005. Natl Vital Stat Rep 2009;57:1-19.

2. Silver RM. Fetal death. Obstet Gynecol 2007;109:153-6. 3. Cunningham FG, Gant NF, Leveno KJ, Gilstrap LC, Hauth

JC, Wenstrom KD. Fetal death. In: Cunningham FG, edi-tor. Williams obstetrics. NewYork: Mc Graw-Hill; 2001. p.1073-8:

4. Fretts RC. Etiology and prevention of stillbirth. Am J ObstetGynecol 2005;193:1923-35.

5. Luna F, Polo V, Fernandez-Santander A, Moral P. Stillbirthpattern in an isolated Mediterranean population. Hum Biol2001;73:561-73.

6. Önderoglu L, Tuncer ZS. The clinical predictors ofintrauterine fetal death. Turk J Pediatr 1998;40:543-7.

7. Kale A, Akdeniz N, Erdemoglu M, Yal›nkaya A, Yayla M.On y›ll›k 660 ölü do¤um olgusunun retrospektif analizi.Perinatoloji Dergisi 2005;13:101-4.

8. Cnattingius S, Bergstrom R, Lipworth L, Kramer MS.Prepregnancy weight and the risk of adverse pregnancy out-comes. N Engl J Med 1998;338:147-52.

9. Stephansson O, Dickman PW, Johansson A, Cnattingius S.Maternal weight, pregnancy weight gain, and the risk ofantepartum stillbirth. Am J Obstet Gynecol 2001;184:463-9.

10. Faye-Petersen OM, Guinn DA, Wenstrom KD. Value ofperinatal autopsy. Obstet Gynecol 1999;94:915-20.

11. Pauli RM, Reiser CA. Wisconsin Stillbirth Service Program:II. Analyses of diagnoses and diagnostic categories in the first1,000 referrals. Am J Med Genet 1994;50:135-53.

12. Copper RL, Goldenberg RL, DuBard MB, Davis RO. Riskfactors of fetal death in white, black and Hispanic women.Obstet Gynecol 1994;94:490-5.

13. Madazl› R, Uluda¤ S, Aksoy F, fien C, Ocak V. CerrahpaflaT›p Fakültesi Kad›n Hastal›klar› ve Do¤um Klini¤inde1986-1992 y›llar› aras›ndaki perinatal otopsi olgular›n›n ird-elenmesi. Perinatoloji Dergisi 1994;2:94-100.

14. Gürel H, Atar Gürel S, Kamac› M. Klini¤imizdeki perinatalölüm olgular›n›n de¤erlendirilmesi. Türkiye KlinikleriJinekoloji-Obstetrik 1998;8:69-73.



139

Investigation of the relationship between levels ofoxidative stress markers in the second trimester

amniotic fluid with preeclampsia and preterm deliveryEbru Çelik1, Abdullah Karaer1, Ercan Y›lmaz1, Ilg›n Türkçüo¤lu1, Önder Çelik1, Yavuz fiimflek1,

P›nar K›r›c›1, Elif Özerol2, Kevser Tanbek2

1Department of Obstetrics and Gynecology, Faculty of Medicine, ‹nönü University, Malatya, Turkey2Biochemistry Department, ‹nönü University Turgut Özal Research Center, Malatya, Turkey

Abstract

Objective: To determine whether concentrations of oxidativestress markers of amniotic fluid are different in healthy pregnantwomen from pregnant women with either preeclampsia orpreterm birth before 34 weeks gestation. Methods: This was a retrospective cohort study consisting of con-secutive 182 pregnant women with singleton gestations undergoingmidtrimester amniocentesis for clinical indications (advancedmaternal age, abnormal screening tests for trisomies or maternalrequest) in ‹nonü University, Turgut Özal Research Centerbetween April 2011 and May 2012. Patients were invited to donateamniotic fluid for research purposes. The pregnancy outcome wascollected by reviewing the charts of hospital or by contacting thepatients. Exclusion criteria from the study were: (i) incomplete dataabout the outcome of pregnancy, (ii) confirmed fetal abnormalitiesor chromosomal abnormalities, (iii) presence of intrauterine infec-tion, (iv) maternal systemic diseases such as chronic hypertension ordiagnosis of gestational diabetes mellitus. Amniotic fluid sampleswere obtained by transabdominal amniocentesis and 4-5 mL wascollected for research purposes. Amniotic fluid samples were storedat -80°C for the future analysis. Diagnosis of preeclampsia was madeaccording to the criteria of International Society for the Study ofHypertension in Pregnancy. Results: The mean amniotic fluid concentrations of SOD, ADA,MPO, XO and MDA were not different in the preeclamptic groupfrom the control group. Further, the mean concentrations ofSOD, ADA, MPO, XO and MDA in the preterm group were alsosimilar to those in the normal healthy pregnant women.Conclusion: The oxidative stress markers appear not to be differ-ent among the groups. The relation of preterm birth andpreeclampsia with oxidative stress and its implication in amnioticenvironment need to be addressed in further studies. Key words: Oxidative stress, preeclampsia, preterm birth, amni-otic fluid.

‹kinci trimesterde amniyotik s›v›da oksidatif stresbelirteçlerinin düzeyleri ile preeklampsi geliflimi veerken do¤um aras›ndaki iliflkinin araflt›r›lmas›Amaç: Oksidatif stres belirteçlerinin amniyon s›v›s›ndaki konsan-trasyonlar›n›n sa¤l›kl› gebeler ile preeklampsi veya 34 haftadan ön-ce erken do¤um komplikasyonu geliflen gebeler aras›nda karfl›lafl-t›rmak.Yöntem: Bu çal›flma Nisan 2011 ve May›s 2012 tarihleri aras›nda‹nönü Üniversitesi Turgut Özal Araflt›rma Merkezi’nde klinik endi-kasyonu (ilerlemifl anne yafl›, trizomiler için anormal görüntülemetestleri veya anne iste¤i) olan gebelere midtrimester amniyosentezyap›ld›. Tekiz gebeli¤i olan toplam 182 kad›n› içeren retrospektif birkohort çal›flmas› olan bu çal›flmada hastalar, araflt›rma amaçl› olarakamniyotik s›v› ba¤›fllamaya davet edildiler. Gebelik sonucu, hastanedosyalar›ndan veya hastalara telefon ile ulaflarak topland›. Çal›flmad›fl›nda kalma kriterleri; (i) gebeli¤in sonucu hakk›nda eksik veri, (ii)fetal veya kromozomal anomaliler, (iii) intrauterin enfeksiyon varl›-¤›, (iv) kronik hipertansiyon gibi maternal sistemik hastal›klar veyagestasyonel diabet geliflmesi idi. Amniyotik s›v› örnekleri ultraso-nografi eflli¤inde transabdominal yolla al›nd› ve araflt›rma amac›yla4-5 mL topland› ve analiz için -80°C’de sakland›. Preeklampsi tan›-s›, “International Society for the Study of Hypertension in Preg-nancy” kriterlerine göre yap›ld›. Bulgular: SOD, ADA, MPO, XO ve MDA’n›n ortalama amniyo-tik s›v› konsantrasyonlar› preeklamptik grupta kontrol grubunagöre farkl› de¤ildi. Buna ek olarak, SOD, ADA, MPO, XO veMDA’n›n ortalama konsantrasyonlar› erken do¤um grubunda danormal sa¤l›kl› gebe kad›nlarla benzer olarak bulundu. Sonuç: Oksidatif stres belirteçleri gruplar aras›nda farkl› bulun-mad›. Erken do¤um ve preeklampsi ile oksidatif stresin amniyotikçevredeki etkisi, baflka çal›flmalarla incelenmelidir.

Anahtar sözcükler: Oksidatif stres, preeklampsi, erken do¤um,amniyotik s›v›.

Correspondence: Ebru Çelik, MD. ‹nönü Üniversitesi Turgut Özal T›p Merkezi, Malatya, Turkey.e-mail: [email protected]

Received: October 18, 2012; Accepted: December 13, 2012




Research Article


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Investigation of the relationship between levels of oxidative stress markers in the second trimester amniotic fluid

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IntroductionOxidative stress plays a key role in the pathophysiolo-gy of placenta-related disorders, particularlypreeclampsia (PE) and premature delivery.[1] Pre-eclampsia, which is associated with an increased prena-tal and maternal mortality and morbidity, occurs inabout 2% of pregnancies.[2,3] Even though the patho-genesis of pre-eclampsia has still been unclear, defec-tive antioxidant activity may damage vascular endothe-lium and result in clinical symptoms of preeclampsia(4). Increased levels of oxidative stress and low levels ofwater-soluble and fat-soluble antioxidants in the plas-ma have been demonstrated in pregnancy disorderssuch as preeclampsia and preterm birth.[5,6] In pretermbirth, oxidative stress is asserted to cause impairmentof collagen through increased reactive oxygen speciesor antioxidant depletion.[7] Growing evidence suggeststhat oxidative stress is involved in the pathogenesis ofpregnancy disorders associated with placentalischemia, responsible for abnormal placentation.[8,9]

The purpose of this study was to compare thedegree of oxidative stress in normal pregnancies and in

pregnancies complicated with pre-eclampsia and pre-mature births before 34 weeks gestation. We measuredantioxidant enzyme activity (superoxide dismutase,adenosine deaminase, myeloperoxidase and xanthineoxide) and free radicals (malondialdehyde). We aimedto potentially determine pregnant women at risk ofobstetric complications through the assessment ofoxidative stress.

MethodsThis was a retrospective cohort study consisting ofconsecutive 182 pregnant women with singleton gesta-tions undergoing midtrimester amniocentesis for clin-ical indications (advanced maternal age, abnormalscreening tests for trisomies or maternal request) in‹nonü University, Turgut Özal Medical Centrebetween April 2011 and May 2012. The follow-upchart of participants was presented in Fig. 1.

Patients were invited to donate amniotic fluid forresearch purposes. The pregnancy outcome was col-lected by reviewing the charts of hospital or by con-

Patient record flow scheme

182 patients applied for amniocentesis

Gestational result wasnot reached (n=44)

Those accepted to participate to the study (n=141)

97 pregnants were suitable for the study

Normal healthy pregnants (n=71) Preterm birth (n=15) Preeclampsia group (n=11)

Those excluded from the study (n=54)• Systemic disease (n=12)• Fetal intrauterine infection and grawth retardation (n=9)• Fetal chromosomal anomaly (n=7)• Fetal major defect (n=8)• Fetal loss before 24 weeks gestation (n=2)• Unappropriate amniotic fluid (n=16)

Fig. 1. Patient record scheme.

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tacting the patients. The collection of samples andclinical data was approved by the Institutional ReviewBoards of Inonu University (Protocol no: 2012/113,17/07/2012). Written informed consent forms wereobtained from all patients. Exclusion criteria from thestudy were: (i) incomplete data about the outcome ofpregnancy, (ii) confirmed fetal abnormalities or chro-mosomal abnormalities, (iii) presence of intrauterineinfection, and (iv) maternal systemic diseases such aschronic hypertension or diagnosis of gestational dia-betes mellitus.

Amniotic fluid samples were obtained by transab-dominal amniocentesis and 4-5 mL was collected forresearch purposes. Amniotic fluid samples were storedat -80°C for the future analysis. Diagnosis of PE wasmade according to the criteria of International Societyfor the Study of Hypertension in Pregnancy.[10] PE ischaracterized by systolic blood pressure ≥140 mmHgand/or diastolic blood pressure ≥90 mmHg on at leasttwo occasions with 4 hour of intervals developing after20 weeks gestation in previously normotensive womenwith proteinuria of above 300 mg in 24 hours (or atleast two positive readings on dipstick analysis of mid-stream urine specimens if no available 24-h collectionof urine). Spontaneous delivery was defined as vaginaldelivery without induction of labor or Cesarean sectionfollowing spontaneous onset of labor. Althoughpreterm delivery is classically defined as birth before 37weeks gestation, we used 34 weeks gestation becausefetal lung maturation is completed at 34 weeks gesta-tion.

Biochemical analyses

In order to evaluate the prooxidant–antioxidant bal-ance, the free radicals production were determined bymeasuring of lipid peroxidation (MDA) levels. Assayswere conducted blind to clinical information. The bio-chemist was blinded to the samples. The amniotic fluidwas extracted with an equal volume of an ethanol/chlo-roform mixture (5:3, volume per volume [v/v]). Aftercentrifugation at 5000 x g for 30 min, the clear upperlayer (the ethanol phase) was collected and used in theSOD activity assay. All preparation procedures wereperformed at 4°C. Total (Cu–Zn and Mn) SOD (EC1.15.1.1) activity was determined according to themethod of Sun.[11] Amniotic fluid adenosine deaminase(ADA) activity was estimated spectrophotometricallyby the method of Giuisti,[12] which is based on the indi-rect measurements of the formation ammonia, pro-

duced when ADA acts in excess of adenosine. Xanthineoxidase (XO) (EC 1.2.3.2) activity was assayed spec-trophotometrically by the formation of uric acid fromxanthine through the increase in absorbance at 293nm.[13] One unit of activity was defined as 1 μmol uricacid formed per minute at 37°C with pH 7.5.Malondialdehyde level was determined by a method ofEsterbauer and Cheeseman.[14] based on the reactionwith thiobarbituric acid (TBA) at 90-100°C. In theTBA test reaction, malondialdehyde (MDA) or MDA-like substances and TBA react with the production of apink pigment having an absorption maximum at 532nm. The reaction was performed at pH 2-3 at 90°C for15 min. The sample was mixed with two volumes ofcold 10% (w/v) trichloroacetic acid to precipitate pro-tein. The precipitation was pelleted by centrifugation,and an aliquot of the supernatant was reacted with anequal volume of 0.67% (w/v) TBA in a boiling waterbath for 10 min. After cooling, the absorbance was readat 532 nm. The results were expressed according to astandard graphic that was prepared on the basis of astandard solution (1, 1, 3, 3-tetramethoxypropane).

Statistical analysis

Data distribution was tested using the Kolmogorov-Smirnov test. Comparison among the outcome groupswas performed using the chi-square test for categoricalvariables and Mann-Whitney U tests for continuousvariables. Data were presented as mean and standarddeviation (SD) for continuous variables and as n (%)for categorical variables. The statistical software pack-age SPSS 19.0 (SPSS Inc., Chicago, IL, USA) was usedfor data analyses.

ResultsThe clinical and obstetrical characteristics of womenwith uncomplicated pregnancies (control, n=71), pre-eclampsia (n=15) and premature delivery (n=11) aredisplayed in Table 1. As expected, the normal preg-nant women had a higher mean gestational age andbirth-weight at delivery than preeclamptic group(p<0.001 and p<0.001, respectively) and preterm group(p<0.001 and p<0.001, respectively) (Table 1). Therewere no significant differences between women withpregnancy complications and uncomplicated pregnan-cies regarding to demographic characteristics. The val-ues of serum ADA, SOD, MDA and XO in womenwith pre-eclampsia and with preterm birth were not



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statistically different from the controls (Table 2). Thevalues of MPO in the pathological pregnancies and inthe preterm labor were also similar to the controlgroup (p=0.59).

DiscussionIn this study, we have observed similar values of oxida-tive stress indicators in amniotic fluid samples obtainedat midtrimester in women who subsequently developedpreeclampsia and delivered prematurely comparedwith women who delivered without any gestationalcomplication. Likewise, similar amniotic fluidmyeloperoxidase concentrations were noted in womenwith complicated pregnancies and control group. Anuncomplicated pregnancy is a pro-oxidant state, whichis characterized with equilibrium between free antioxi-dants and oxidative stress. Oxidative stress has beenpreviously proposed as a mediator of preterm birth, butbiomarkers of oxidative stress have not been noted ineither amniotic fluid of preterm or term pregnancies.

Although there is an imbalance between antioxidantactivity and oxidative stress markers as gestationadvances, antioxidant production decreases when ges-tation achieves term.[15,16] Therefore, in this study, weattempted to prove that oxidative stress biomarkers inamniotic fluid could be an indicator for pathologicalpregnancies. However, we observed no differences inthe concentrations of oxidative stress between preg-nancies developing preeclampsia and resulting withpreterm birth and uncomplicated pregnancies.

It has been demonstrated that antioxidants can bemeasured in the amniotic fluid, but in much lower con-centrations compared to serum.[17] The explanation ofthe discrepancy of our findings with the previous stud-ies may be that we did not evaluate the serum concen-trations of antioxidants. Several studies have noted theassociation of maternal oxidative stress biomarkers atthe early pregnancy with pregnancy complications. Astudy on longitudinal analysis serum samples obtainedfrom 18-22 weeks gestation until birth of baby at 4week intervals has demonstrated a trend tending to

Table 1. Comparison of clinical and obstetric characteristics between study groups developing gestational complications andthe control group.

Preeclampsia group Uncomplicated pregnancies Preterm delivery(n=11) (n=71) (n=15)

Maternal age 33.18±5.36 32.66±5.69 35.07±2.58

Nulliparity 7 (63.6%) 21 (29.6%) 2 (13.3%)

Gestational age at amniocentesis (weeks) 18.55±1.21 18.30±1.21 18.75±1.29

Gestational age at delivery (weeks) 32.36±3.20 37.85±1.70 30.47±2.59

Birth-weight (g) 1959.55±836.96 3114.30±461.30 1680.73±562.38

Male neonates 6 (54.5%) 33 (46.5%) 7 (46.7%)

Table 2. Comparison of the oxidative stress biomarkers among the study and control groups.

Oxidative stress Preeclampsia Preterm Birth Controlsbiomarkers (n=11) (n=15) (n=71) P1 P2

MPO (mU/g protein) 12.57±6.36 11.14±2.89 12.92 ±8.22 0.77 0.85

SOD (U/mg protein) 0.29±0.18 0.33±0.28 0.28±0.17 0.91 0.80

XO (U/g protein) 0.96±0.59 0.85±0.55 1.07±0.73 0.95 0.64

ADA (U/g protein) 0.09±0.09 0.07±0.10 0.05±0.035 0.34 0.39

MDA (nmol/g protein) 0.49±0.42 0.52±0.40 0.43±0.38 0.65 0.82

Measurements of various oxidative stress markers, including amniotic fluid SOD, MPO, XO, ADA and MDA activity at 16 to 21 weeks gestation inwomen who developed subsequent pregnancy complications and those with uncomplicated pregnancies. The values are represented as mean andstandard deviation. P1 value was presented for comparison between women with uncomplicated pregnancies and those with preeclampsia. P2 val-ues were presented for comparison between women with uncomplicated pregnancies and those with preterm birth.

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increase concentrations of oxidative stress markers inpregnancies complicated with preeclampsia.[17]

A recent meta-analysis has reported that serumconcentrations of MDA, an end-product of lipid per-oxidation, were significantly higher in pregnanciescomplicated with preeclampsia when compared tothose in normal pregnancies.[18] However, Bogavac etal. found contradicting results that MDA levels werelow in amniotic fluid of women with preeclampsia.[19]

We noted concentrations of MDA and XOD inwomen with complicated pregnancies were similar tothose with normal pregnancies, which is not in corre-lation with alteration of oxidative stress in the pregnan-cies with preeclampsia.[18,19] Additionally, levels of SOD,intracellular enzyme of antioxidative defense, remainalike in the women with complicated pregnancies,which is in agreement with the previous study.[19,20] Theconcentrations of ADA, which is present in all humantissue and regarded as a cellular inflammatory indica-tor, were previously detected higher in plasma ofwomen with preeclampsia than normal healthy preg-nancies.[21] However, our result again was not in accor-dance with published literature data. The explanationof this discrepancy may be that we did not measureplasma levels of ADA and the gestational week of sam-ple collection was different from the previous study.

Oxidative stress has been suggested to be one of themain pathological processes involved in the pretermpremature rupture of membrane (PPROM). The asso-ciation of endogenous antioxidant status with prema-ture rupture of membrane was studied. The plasmalevels of MDA were found to be higher, and SOD andGSH were lower in women with PPROM than thosein healthy subjects.[22] There were, however, a conflict-ing results reported by Hsieh et al. that there were nodifferences in the plasma levels of SOD activitybetween women with uncomplicated pregnancies andthose who delivered prematurely.[20] We also found thatthe levels of antioxidants and lipid peroxidation in thepremature birth group were similar to those in thehealthy control group, which is in line with the previ-ous data.

There are some limitations in the current study.First, in this study, we recruited participants at 19 to 21weeks gestation when they were screened for pretermbirth. It is arguable that this timing of examinationwould be early for investigating the pathophysiology ofpreterm birth. Second, we did not assess the placentas.

However, all amniotic fluid had been collected in thishospital, but the majority of study population did notdeliver in the same institution and as a consequence, itwas not possible to obtain an adequate number of pla-centas for investigating the role of oxidative stress inthe underlying pathology of complicated pregnancy.Third limitation is a relatively small number ofpatients. The lack of these statistically significant find-ings between study and control groups for a relativelycommon finding raises possibility that the resultoccurred due to a Type I (alpha) error. Further, thestudy was underpowered (<80%) to detect a differencein oxidative stress biomarkers, as having 11 and 15patients in the study groups.

ConclusionIn summary, we did not find any differences in oxida-tive stress biomarkers between women with uncompli-cated pregnancies and those who subsequently devel-oped pregnancy complications. This study may suggestthat the oxidative stress markers appears not to haveearly impact on the development of pregnancy relatedcomplications, but considering our findings, it is diffi-cult to state the implication of high oxidative stress onthe pathogenesis of pregnancy related complications.Nevertheless, future studies are required to examinewhether biomarkers of oxidative stress in amnioticfluid can be used as a screening to determine pregnantwomen at a high risk for those complications.


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tive stress in spontaneous abortion and recurrent pregnancyloss: a systematic review. Obstet Gynecol Survey2007;62:335-47.

2. WHO. Make every mother and child count. Geneva: WHO;2005.

3. Cantwell R, Clutton-Brock T, Cooper G, et al. SavingMothers’ Lives: reviewing maternal deaths to make mother-hood safer: 2006–2008. The Eighth Report of theConfidential Enquiries into Maternal Deaths in the UnitedKingdom. BJOG 2011;118 Suppl 1:S1-S203.

4. Sa¤ol S, Ozkinay E, Ozflener S. Impaired antioxidant activi-ty in women with preeclampsia. Int J Gynaecol Obstet1999;64:121-7.

5. Krishna Mohan S, Venkataramana G. Status of lipid peroxi-dation, glutathione, ascorbic acid, vitamin E and antioxidant



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enzymes in patients with pregnancy-induced hypertension.Indian J Physiol Pharmacol 2007;51:284-8.

6. Longini M, Perrone S, Vezzosi P, et al. Association betweenoxidative stress in pregnancy and preterm premature ruptureof membranes. Clin Biochem 2007;40:793-7.

7. Wall PD, Pressman EK, Woods JR Jr. Preterm prematurerupture of the membranes and antioxidants: the free radicalconnection. J Perinatal Med 2002;30:447-57.

8. Abrahams VM, Kim YM, Straszewski SL, Romero R.Mor G.Macrophages and apoptotic cell clearance during pregnancy.Am J Reprod Immunol 2004;51:275-82.

9. Sargent IL, Germain SJ, Sacks GP, Kumar S, RedmanCW.Trophoblast deportation and the maternal inflammato-ry response in preeclampsia. J Reprod Immunol2003;59:153-60.

10. Davey DA, MacGillivray I. The classification and definitionof the hypertensive disorders of pregnancy. Am J ObstetGynecol 1988;158:892-8.

11- Sun Y, Oberley LW, Li Y. A simple method for clinical assayof superoxide dismutase. Clin Chem 1988;34:497-500.

12. Giusti G. Adenosine deaminase. In: Bergmeyer MV, editor.Methods of enzymatic analysis. 2nd ed. New York: AcademicPress; 1974. p. 1092-8.

13. Prajda N, Weber G. Malignant transformation-linkedimbalance: decreased xanthine oxidase activity in hepatomas.FEBS Lett 1975;59:245-9.

14. Esterbauer H, Cheeseman KH. Determination of aldehydiclipid peroxidation products: malonaldehyde and 4-hydrox-ynonenal. Methods Enzymol 1990;186:407-21.

15. Gitto E, Reiter RJ, Karbownik M, Tan DX, Gitto P, BarberiS, et al. Causes of oxidative stress in the pre- and perinatalperiod. Biol Neonate 2002;81:146-57.

16. Watson AL, Palmer ME, Jauniaux E, Burton GJ. Variationsin expression of copper/zinc superoxide dismutase in villoustrophoblast of the human placenta with gestational age.Placenta 1997;18:295-9.

17. Chappell LC, Seed PT, Briley A. A longitudinal study ofbiochemical variables in women at risk of preeclampsia. AmJ Obstet Gynecol 2002;187:127-36.

18. Gupta S, Aziz N, Sekhon L. Lipid peroxidation and antioxi-dant status in preeclampsia: a systematic review. ObstetGynecol Surv 2009;64:750-9.

19. Bogavac M, Lakic N, Simin N, Nikolic A, Sudji J, Bozin B.Biomarkers of oxidative stress in amniotic fluid and compli-cations in pregnancy. J Matern Fetal Neonatal Med2012;25:104-8.

20. Hsieh TT, Chen SF, Lo LM, Li MJ, Yeh YL, Hung TH.The association between maternal oxidative stress at mid-gestation and subsequent pregnancy complications. ReprodSci 2012;19:505-12.

21. Karabulut AB, Kafkasli A, Burak F, Gozukara EM. Maternaland fetal plasma adenosine deaminase, xanthine oxidase andmalondialdehyde levels in pre-eclampsia. Cell BiochemFunct 2005;23:279-83.

22. Yin B, Zhen M. Lipid peroxidation in plasma and the activi-ty of superoxide dismutase (SOD) in pregnant women withpremature rupture of membrane. Zhonghua Yi Xue Za Zhi1995;75:463-5, 509.

Ovarian cyst rupture during real-time transvaginalDoppler ultrasonography

Mekin Sezik

Department of Obstetrics and Gynecology, Faculty of Medicine, Süleyman Demirel University, Isparta, Turkey

IntroductionIn acute pelvic pain cases, transvaginal ultrasonography(TV-USG) becomes the most essential and practicalexamination method. TV-USG also has a specialimportance in differential diagnosis of gynecologic andother etiologies of women who refer to clinics forpelvic pain.[1] TV-USG is also required for distinguish-ing normal intrauterine pregnancies from cases such asabort or ectopic pregnancy. Becoming widespread andportable of ultrasonography devices and decrease ofcosts makes TV-USG a standard for the examinationof pelvic pain especially of women who are sexuallyactive.[2]

Usually, Doppler is a routine option offered in ultra-sonography devices released to the market especiallyduring the last decade. Sonographic color Doppler prac-tices also can be used for differential diagnosis of differ-ent pelvic pathologies. For example, hemorrhagic cor-pus luteum cysts that may cause pelvic pain are revealedby peripheral Doppler blood flow with low vascularresistance.[3,4] This typical “fire circle” view mostly helpsto establish diagnosis. Therefore, using color Dopplerduring TV-USG –at least in some cases– is expected toincrease diagnostic precision.

In this study, we presented a “simple” ovarian cystrupture during TV-USG in a women referred to us for

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Abstract

Objective: To present a case of ovarian cyst rupture during trans-vaginal Doppler ultrasound examination.

Case: A 46-year-old woman with abdominal pain referring toright groin was evaluated with abdominal ultrasonography andpresented at our clinic due to a hypoechoic, nonseptated ovariancyst with regular borders of approximately 7 cm in diameter.Following abrupt and intense pelvic pain starting with the trans-vaginal scan, the color Doppler revealed high velocity and irregu-lar flow from the posterior cervicouterine wall toward the Pouchof Douglas; then, the patient’s pain rapidly regressed.

Conclusion: To the best of our knowledge, this is the first reportrevealing real-time spontaneous rupture of a “simple” ovarian cystduring Doppler sonography.

Key words: Ovarian cyst rupture, Doppler ultrasonography.

Gerçek zamanl› transvajinal Doppler ultrasonografiesnas›nda over kist rüptürüAmaç: Transvajinal Doppler ultrasonografik muayene s›ras›ndagerçekleflen over kist rüptürünün sunulmas›.

Olgu: Sa¤ kas›¤›na vuran kar›n a¤r›s› nedeni ile abdominal ultra-sonografi ile de¤erlendirilen 46 yafl›ndaki kad›n hastada yaklafl›k 7cm pelvik çap›nda düzgün cidarl›, hipoekoik, septas›z over kistisaptanmas› üzerine klini¤imize sevk edilmiflti. Transvajinal ultra-sonografi bafllang›c›nda, ani ve keskin a¤r› ile servikouterin arkaduvardan Douglas bofllu¤una do¤ru h›zl› ve düzensiz Dopplerak›m saptand›; sonras›nda, hastan›n a¤r›s› h›zla geriledi.

Sonuç: Ulaflabildi¤imiz kadar› ile “basit” over kistinin spontanerüptürü ilk kez gerçek zamanl› olarak, Doppler ultrasonografi ilekay›t alt›na al›nm›fl olmaktad›r.

Anahtar sözcükler: Over kist rüptürü, Doppler ultrasonografi.

Correspondence: Mekin Sezik, MD. Süleyman Demirel Üniversitesi T›p Fakültesi Kad›n Hastal›klar› ve Do¤um A.D. 32260 Isparta, Turkey.e-mail: [email protected]

Received: November 10, 2012; Accepted: November 28, 2012





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acute pelvic pain. Color Doppler diagnoses duringultrasonographic examination were also recorded. Asfar as we accessed through ULAKB‹M TurkishMedicine Index, PubMed, Scopus and GoogleAcademic Internet database, there is no record aboutreal-time display of ovarian cyst rupture. Based on ourcase report, we have discussed up-to-date data on ovar-ian cyst ruptures.

Case ReportA 46-year-old woman (gravida 3, para 2) referred tothe emergency service of our hospital due to bottomquadrant pain referring to right groin on 22nd day ofmenstrual cycle. In her transabdominal ultrasonogra-phy, 68x72 mm cystic mass defined as “simple” wasfound on right adnexal area which had regular borders,in hypoechoic appearance and was nonseptated. Then,consultation was requested from the Department ofObstetrics and Gynecology.

There were 2 normal vaginal deliveries without anycomplication in the anamnesis of the patient, it wasstated that her menarche age was 15 and her menstru-al periods were regular (lasting for 5 days with 27 daysof intervals). There was no significant characteristic orsurgery in obstetric and gynecologic anamnesis of thepatient. Full blood count, routine blood biochemistryvalues and full urine examination parameters of patient

during admittance were found within normal ranges.Serum beta-hCG (human chorionic gonadotrophin)value was 3 mIU/mL (values below 10 mIU/mL werenegative). The patient did not mention about any aller-gy history.

First, TV-USG examination was planned due tothe consultation reason. In TV-USG examination (5-8mHz multi-frequency vaginal probe, Voluson Expert,GE Healthcare, Zipf, Austria), hypoechoic ovarian cystwhich was 7 cm in diameter was found in right adnex-al area. Then, color Doppler ultrasonographic exami-nation was performed. However, in the meantime, anabrupt and intense pelvic pain developed. TransvaginalDoppler sonography revealed a rapid and irregularflow from the posterior cervicouterine wall towards thePouch of Douglas (Fig. 1). Secondary “aliasing” arti-facts appeared during turbulence with high velocity(Fig. 2). When rupture cyst content was discharged, aneffusion view appeared gradually within the Pouch ofDouglas which did not exist in the beginning of theexamination (Fig. 3). One minute later, intense pain ofthe patient started to regress. In the meantime, it wasfound that Doppler flow stopped completely. At thisstage, both adnexal areas seemed normal in transvagi-nal imaging; cystic mass in the ovary disappeared andthere was apparent fluid echogenicity in the Pouch ofDouglas.

Fig. 1. Fluid substance begins to discharge into the pouch of Dou-glas rapidly when cyst rupture occurs. Arrow: posterior wallof uterus.

Fig. 2. When cyst content continues to discharge, aliasing artifactsassociated with turbulence flow appear (arrows).

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The patient was hospitalized in the Department ofObstetrics and Gynecology by the diagnosis of “ovari-an cyst rupture”. Her pulse, blood pressure and hema-tocrit follow-ups were carried out once in every sixhours. The patient was discharged with full recoveryafter 48 hours when it was observed that her clinicaland laboratory findings stable. In the check performedfour weeks later, she had normal pelvic and transvagi-nal ultrasonographic findings.

DiscussionThe term “ovarian cyst accidents” is used for bleeding(hemorrhagic) ovarian cysts, ovary torsion, and cystrupture.[5] These “accidents” are seen frequently inclinics. Also, “simple” ovarian cysts are frequently seenespecially during perimenopausal period. In a relative-ly recent autopsy study, this rate was found as 18% inpostmenopausal period;[6] ovarian cyst was foundapproximately in 7% of asymptomatic women between25 and 40 years old during transvaginal ultrasono-graphic examination.[7] In another series where gyneco-

logic acute abdomen cases were evaluated, it wasreported at approximately 22% of applications had atleast one ovarian cyst at or above 5 cm in size.[8]

Ovarian cystic formations with thin wall which areobserved as unilocular, relatively anechoic or hypoe-choic, and do not include septation or papillary struc-ture are called “simple ovarian cyst”. Most of themconsist of anovulatory –and therefore not regressing–ovarian follicles which cannot perform oocyte disposalin menstrual cycle.[9] Mostly, follicles over 25-30 mm indiameter are referred as “cyst”.[10] Sometimes, serous ormucinous ovarian cystadenomas are also may be seenas “simple cyst” as defined above. It is known thatspontaneous rupture develops in some “simple” ovari-an cysts. In such cases, abrupt inferior abdominal painand frequently nausea or vomiting is seen. In our case,nausea or vomiting was not accompanying to intensepain which disturbing the patient noticeably. Actually,beginning characteristics of the pain may be significantfor distinguishing ovarian cyst rupture and ovarian tor-sion cases: while rupture pain is abrupt and mostlyintense, secondary torsion pain is generally gradual.[5]

In ovarian cyst ruptures (unless no bleeding), itshould be expected that severe clinical picture duringrupture rapidly regress, and most patients do not haveany clinical findings except mild peritonism. However,since preshock findings may appear lately in especiallya health woman, it is recommended to follow-up diag-noses such as tachycardia and orthostatic hypoten-sion.[5] We planned hospitalization in our case and fol-lowed-up her vital findings closely; also we evaluatedwhether there was any reduce in her hematocrit values.

Although major persisting follicle cysts are respon-sible for most of the ruptures, benign cystadenomasalso may be ruptured. It is believed that the long-termeffects of serous cyst ruptures are negligible.[5] Eventhough mucinous ovarian cyst ruptures are associatedwith “pseudomyxoma peritonei”, it is agreed that theyare secondary to appendix associated mucinous epithe-lial tumors.[11] Consequently, short-long term progno-sis after “simple” cyst ruptures seems good. It is notknown whether repeating abdominal physical examina-tions or transvaginal ultrasonography increases rupturerisk or not. It is known that functional ovarian cystssometimes cause secondary rupture during excessivephysical activity.[12] However, there is no prospectivedata presenting this association.

Fig. 3. The increased fluid amount in the pouch of Douglas (mar-gins are shown by arrows) is remarkable when current flowslows down. Triangle arrow head: posterior wall of uterus.


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In the emergency medicine literature, ovarian cystruptures following blunt abdominal trauma have beendefined. In one case, severe intraabdominal bleedingsecondary to ovarian dermoid tumor rupture wasdeveloped after car accident.[13] In a recent case report,diagnoses of positive peritoneal lavage secondary to“simple” ovarian cyst rupture were defined which werealso confirmed histopathologically in a 49-year-oldpostmenopausal woman who was passed over by a trac-tor wheel.[14] In another article, an ovarian dermoidtumor case approximately 8 cm in diameter and hadspontaneous rupture during labor was given.[15] Thesefindings show that severe blunt abdominal trauma andeven labor may cause cyst ruptures. However, the casethat abdominal examination even aggressively, ortransvaginal probes may trigger rupture is only basedon assumptions.

In our current case, it can be thought that cyst rup-ture appearing during sonographic examination is onlya coincidence. We could not find any other case reportwhich displayed ovarian cyst rupture by real-timeultrasonography despite comprehensive literature andinternet search. Probably, detailed display of this caseby Doppler technique has been recorded for the firsttime by us. During rupture, we found that fluid cystcontent reaching high velocity enough to create alias-ing was accumulated in posterior “cul-de-sac” also bythe effect of gravity. This explains clinical pictureappearing with abrupt pain in ovarian cyst ruptures.

ConclusionConsequently, findings in the current case show that inthe rupture of “simple” ovarian cysts, cyst fluid mayflow into pelvic cavity in a short time and possible peri-toneal irritation may cause abrupt and intense but tem-porary pain.


References1. Kupesiç S, Aksamija A, Vuciç N, Tripalo A, Kurjak A.

Ultrasonography in acute pelvic pain. [Article in Croatian]Acta Med Croatica 2002;56:171-80.

2. Can M, Güney fi, Öziz E. Transvajinal ultrasonografinintan›sal de¤eri. ‹zmir Atatürk E¤itim ve Araflt›rma HastanesiT›p Dergisi 1998;36:27-32.

3. Tanr›verdi HA, Sade H, Akbulut H, Barut V, Bayar Ü.Pelvik kitlelerin klinik ve ultrasonografik de¤erlendirmesi.Journal of the Turkish German Gynecological Association2007;8:67-70.

4. Timor-Tritsch IE. Tubal ring and corpus luteum echogenic-ities. J Ultrasound Med 2001;20:802.

5. Bottomley C, Bourne T. Diagnosis and management ofovarian cyst accidents. Best Pract Res Clin Obstet Gynaecol2009;23:711-24.

6. Dørum A, Blom GP, Ekerhovd E, Granberg S. Prevalenceand histologic diagnosis of adnexal cysts in postmenopausalwomen: an autopsy study. Am J Obstet Gynecol2005;192:48-54.

7. Borgfeldt C, Andolf E. Transvaginal sonographic ovarianfindings in a random sample of women 25-40 years old.Ultrasound Obstet Gynecol 1999;13:345-50.

8. Haider Z, Condous G, Khalid A, Kirk E, Mukri F, VanCalster B, et al. Impact of the availability of sonography inthe acute gynecology unit. Ultrasound Obstet Gynecol2006;28:207-13.

9. Cicchiello LA, Hamper UM, Scoutt LM. Ultrasound evalu-ation of gynecologic causes of pelvic pain. Obstet GynecolClin North Am 2011;38:85-114.

10. Bourne TH, Hagström H, Hahlin M, Josefsson B, GranbergS, Hellberg P, et al. Ultrasound studies of vascular and mor-phological changes in the human corpus luteum during themenstrual cycle. Fertil Steril 1996;65:753-8.

11. Smeenk RM, Verwaal VJ, Zoetmulder FA. Pseudomyxomaperitonei. Cancer Treat Rev 2007;33:138-45.

12. Ignacio EA, Hill MC. Ultrasound of the acute female pelvis.Ultrasound Q 2003;19:86-98.

13. Levine RL, Pepe PE, Blackstone W, Danzinger J, Varon J.Occult traumatic avulsion of an ovarian dermoid cyst. Am JEmerg Med 1992;10:344-6.

14. Madej B, Fijalkowski P, Burdan F. Post-traumatic rupture ofthe ovarian cyst – case report. Polski Przeglad Chirurgiczny2008;80:630-2.

15. Kumarie R, Machado LS, Krolikowski A. Spontaneous rup-ture of an ovarian tumor during labor. Saudi Med J2002;23:350.

Agenesis of ductus venosus: a case reportTalat Umut Kutlu Dilek1, Burcu Dilek2

1Department of Obstetrics and Gynaecology, Faculty of Medicine, Mersin University, Mersin, Turkey2Radiology Clinic, Private Mersin Yeniflehir Hospital, Mersin, Turkey

IntroductionCirculation system in fetal life is different than postna-tal circulation by 3 shunts included. These are ductusvenosus, foramen ovale and ductus arteriosus. Duringembryonal development period, while right umbilicalvein regresses, an area of left umbilical vein fromentrance point into abdomen to inferior vena cavaendures and is named as ductus venosus. Ductus veno-sus is the shunt responsible for carrying blood, whichhas with high oxygen saturation carried by umbilicalvein, into inferior vena cava. Blood transferred to infe-rior vena cava by this shunt is carried on left dorsal partand reaches right atrium.

The development appeared in ultrasonographytechnique helped to understand anatomy and anom-

alies of fetal venous system better.[1] Ductus venosusagenesis is a rare fetal vascular anomaly. Its prevalenceis reported as 1/2500 according to screening programsperformed between 11 and 14 gestational weeks.[2] Inthis report, ductus venosus agenesis case accompanyingother congenital anomalies found in a pregnantreferred due to abnormal second trimester screeningtest has been discussed.

Case ReportA 27-year-old patient with second pregnancy who hadno obstetric and medical risk factor and referred forurinary anomaly suspect was evaluated. In the secondtrimester screening test of the patient, the risk for neu-ral tube defect was calculated as 1/50 and alpha-feto

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AbstractObjective: Agenesis of ductus venosus is a rare vascular abnormal-ity. We report a of case ductus venosus agenesis, with multipleabnormalities.

Case: Atrioventricular septal defect, right multicystic dysplastickidney, rocker bottom foot, and single umbilical artery weredetected in the anatomic evaluation. It was found that ductusvenosus did not exist and umbilical vein was opening directly toright atrium. Karyotype result was reported as normal constitu-tional karyotype and the pregnancy of the case was terminated dueto multiple congenital anomalies.

Conclusion: Coincidental fetal abnormalities determine progno-sis of ductal agenesis.

Key words: Ductus venosus, agenesis, extrahepatic drainage.

Ductus venosus agenezisi: Olgu sunumuAmaç: Ductus venosus agenezisi nadir bir fetal vasküler anomali-dir. Bu olgu sunumunda, multiple anomalilerle beraber olan duc-tus venosus agenezisi olgusunu bildirdik.

Olgu: Yap›lan anatomik de¤erlendirmede atrioventriküler septaldefekt, sa¤ multikistik displastik böbrek ve ayaklarda rocker bot-tom foot, tek umbilikal arter saptand›. Ductus venosus’un olmad›-¤› umbilikal venin direkt sa¤ atriyuma aç›ld›¤› gözlendi. Karyotipsonucu normal konstitüsyonel karyotip olarak raporlanan olgunungebeli¤i multiple konjenital anomaliler nedeniyle sonland›r›ld›.

Sonuç: Ductus venosus agenezisi vakalar›nda, efllik eden fetal ano-malilerin varl›¤› prognozu belirlemektedir.

Anahtar sözcükler: Ductus venosus, agenezis, ekstrahepatik dre-naj.

Correspondence: Talat Umut Kutlu Dilek, MD. Mersin Üniversitesi E¤itim ve Araflt›rma Hastanesi, Zeytinlibahçe, Mersin, Turkey.e-mail: [email protected]

Received: November 13, 2012; Accepted: December 11, 2012





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protein MoM was reported as 3.21. In the prenatalevaluation of the patient performed when she waspregnant for 19 weeks and 2 days according to her lastmenstrual period, atrioventricular septal defect, rightmulticystic dysplastic kidney, rocker bottom footdeformity on foot, and single umbilical artery weredetected in fetus of which biometric measurementswere consistent with 18 weeks and 5 days. It wasobserved that ductus venosus did not exist and umbili-cal vein was directly opened to right atrium by display-ing extrahepatic drainage (Figs. 1 and 2). Geneticamniocentesis was done to the patient due to thesediagnoses.

Karyotype result was reported as normal constitu-tional karyotype. Due to the existing multiple congen-ital anomalies, termination of pregnancy was recom-mended to the patient. Upon the acceptance of thepatient, the pregnancy was terminated at 22 gestation-al weeks. Postmortem examination was not done sincethe patient did not accept.

DiscussionDuctus venosus is an anatomic shunt in intrauterinelife providing connection between umbilical vein andinferior vena cava. It turns into ligamentum venosumafter delivery. In the existence of ductus venosus,

umbilical vein may be opened directly into intrahepat-ic left portal vein, iliac vein, inferior vena cava, andright atrium.[3] It was reported that progressive cardiacdecompensation and hydrops fetalis are seen muchmore in extrahepatic insertions (right atrium, vena cavainferior etc.) of ductus venosus.[3,5]

Shen et al.[6] reported that in ductus venosus agene-sis cases where extrahepatic drainage is seen, portal sys-tem is developed if shunt diameter is small and portalsystem is not developed if shunt is has a diameter samewith or wider than umbilical vein. Non-existence ofductus venosus may be accompanied with hydrops, car-diac, (ASD, VSD, major vascular transposition, rightventricle with dual outlet, non-existence of inferiorvena cava, pulmonary arterial anomalies), renal anom-alies (hypoplasia, agenesis), cleft palate, hypospadias,mesomelic karyotype anomalies (Turner, Noonan,Trisomy 22, other subchromosomal disorders).[3,7-9]

Since associated karyotype anomaly reaches up to 25%in some series, it can be recommended to carry outkaryotyping in cases with ductus venosus agenesis.[10]

In a series of 22 cases, it was reported by Thomas etal.[7] that perinatal loss and pregnancy termination ratewas 45% in cases accompanied by structural anomaly,and it was 75% in cases accompanied by chromosomalanomaly while survival rate was 100% in isolated cases.

Fig. 1. The course of umbilical vein beginning from the inlet point into abdomen anddirect opening to right atrium.

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Berg et al.[3] reported that prognosis varied according tointrahepatic or extrahepatic drainage of umbilical veinand it was worse in those with extrahepatic drainage.Survival rate was 100% in ductus venosus agenesis caseswhere isolated, hydrops and pleural effusion did notaccompanied; otherwise, the rate was reduced to 50%.[7]

In our case, hydrops was not observed; however, accom-panying cardiac and renal anomalies and existence ofsingle umbilical artery were consistent with the casereports and cases series reported in the literature.

ConclusionIncreasingly examining ductus venosus by ultrasono-graphic evaluations performed during aneuploidyscreenings between 11 and 14 gestational weeks enabledto establish ductus venosus agenesis diagnosis more. Yet,it is a malformation rarely observed. Portal venous sys-tem should also be evaluated in case of extrahepaticdrainage of umbilical vein as well as full anatomic evalu-ation and karyotyping in cases diagnosed ductus venosusagenesis. Existence of hydrops and accompanyinganomalies are major factors determining prognosis.


References1. Yagel S, Kivilevitch Z, Cohen SM, Valsky DM, Messing B,

Shen O, et al. The fetal venous system, part I:normalembriyology, anatomy, hemodynamics, ultrasound evalua-tion and doppler investigation. Ultrasound Obstet Gynecol2010;35:741-50.

2. Stabulidau I, Pereira S, de Jesus Cruz J Syngelaki A,

Nicolaides KH. Prevalence and outcome of absence ductusvenosus at 11(+0) to 13(+6) weeks. Fetal Diagn Ther2011;30:35-40.

3. Berg C, Kamil D, Geipel A, Kohl T, Knöpfle G, HansmannM, et al. Absence of ductus venosus–importance of umbilicalvenous drainage site. Ultrasound Obstet Gynecol2006;28:275-81.

4. Contratti G, Banzi C, Ghi T, Perolo A, Pilu G, Visentin A.Absence of the ductus venosus: report of 10 new cases andreview of the literature. Ultrasound Obstet Gynecol2001;18:605-9.

5. Jaeggi ET, Fouran JC, Hornberger LK, Proulx F,Oberhänsli I, Yoo SJ, et al. Agenesis of the ductus venosusthat is associated with ex-trahepatic umbilical vein drainage:prenatal features and clinical outcome. Am J Obstet Gynecol2002;187:1031-7.

6. Shen O, Valsky DV, Messing B, Cohen SM, Lipzschuetz M,Yagel S. Shunt diameter in agenesis of the ductus venosuswith extrahepatic portosystemic shunt impact on prognosis.Ultrasound Obstet Gynecol 2011;37:184-90.

7. Thomas JT, Petersen S, Cincotta R, Lee-Tannock A,Gardener G. Absent ductus venosus -outcomes and implica-tions from tertiary center. Prenat Diagn 2012;32:686-91.

8. Corbacioglu A, Aslan H, Dagdeviren H, Ceylan Y. Prenataldiagnosis of abnormal course of umbilical vein and ductusvenosus agenesis: report of three cases. J Clin UltrasoundPrenat Diagn 2012:40;590-3.

9. Clerici G, Rosati A, Di Renzo GC. Absent ductus venosusassociated with skeletal anomalies of the ulna and radius.Prenat Diagn 2010;32:83-5.

10. Volpe P, Marasini M, Caruso G, Lituania M, Marzullo A,Volpe G, et al. Prenatal diagnosis of ductus venosus agenesisand its association with cytogenetic/congenital anomalies.Prenat Diagn 2002;22:995-1000.

Fig. 2. Direct opening of umbilical vein into right atrium and inferior vena cava joining to the same point from posterior in color-flow mode.

Sonographically documented spontaneous resolutionof isolated fetal ascites

fiad›man K›ykaç Alt›nbafl, Ömer Kandemir, Serdar Yalvaç, Ümit Göktolga

Clinic of Obstetrics and Gynecology, Etlik Zübeyde Han›m Gynaecology Training and Research Hospital, Ankara, Turkey

IntroductionDiagnosis of isolated fetal ascites during antenatal fol-low-up is a rare case and it is usually associated with apathology. Cardiac, genitourinary, gastrointestinal,respiratory, metabolic and infectious reasons are givenin the etiology.[1,2] It is reported that the etiology asso-ciated with the situation is detected in 92% of cases.[3]

Although immune, non-immune hydrops fetalis casesand their reasons are defined well, diagnosis, treatmentand follow-up of isolated fetal ascites are as case reportsin the literature.

In this case report, we aimed to present accordingto the literature the case of isolated fetal ascite whichhad spontaneous remission during antenatal follow-upand to discuss its obstetric management.

Case Report

A 34-year- old patient, who was G3 and P2 and had nokin marriage and no characteristics in family historyand patient history, was referred to our clinic with thepre-diagnosis of fetal abdominal ascites from an exter-

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Abstract

Objective: To present spontaneous resolution of isolated fetalascites diagnosed at antenatal period. Case: A 30-year-old, G3, P2 patient admitted to our perinatologyclinic in 26th week of pregnancy with a diagnosis of severe, isolat-ed fetal ascites without any other anomalies revealed by ultrasoundexamination. The workup for Parvovirus B19, cytomegalovirus,toxoplasmosis, herpes simplex, rubella, hepatitis A, B, C and infec-tious markers were negative. Fetal karyotyping was reported asnormal. As the persistence of fetal ascites was seen at 32 and 34weeks gestation, a complete resolution of the ascites was detectedat 36 weeks’ gestation. A normal 4,200 grams male infant was vagi-nally delivered at 39 weeks gestation. Conclusion: Isolated fetal ascites is a rare ultrasound finding anddiagnosis is to be confirmed with exclusion of related fetal anom-alies, immunologic and nonimmunologic causes. Parents shouldbe counseled about other rare concomitant and undetectableanomalies despite detailed evaluation.Key words: Isolated fetal ascites, ultrasonography.

Ultrasonografik izlemde spontan remisyonau¤rayan izole fetal asit olgu sunusuAmaç: Antenatal dönemde saptanan ve spontan remisyona u¤ra-yan izole fetal asit olgusunun sunulmas›.Olgu: Otuz yafl›nda, G3, P2 olan hasta fetal asit tan›s› ile klini¤i-mize refere edildi. Ultrasonografide 26 hafta ile uyumlu fetal ba-t›nda izole yayg›n asitin efllik etti¤i, ek anomalinin izlenmedi¤i tekcanl› fetus tespit edildi. Hastan›n Parvovirus B19, sitomegalovirus,toksoplazmozis, herpes simpleks, rubella, hepatit A, B, C infeksi-yon belirteçleri negatif saptand›. Karyotiplendirme sonucu normalolarak bildirildi. Hastan›n takipleri s›ras›nda, 32 ve 34. gebelik haf-talar›nda fetal asitin ayn› fliddette devam etti¤i, 36. gebelik hafta-s›nda (2 haftal›k süreçte) fetal asitin tamam›yla spontan redüksiyo-na u¤rad›¤› kaydedildi. Sa¤l›kl›, 4200 gram erkek bebek 39. gebe-lik haftas›nda vajinal yolla do¤urtuldu. Sonuç: ‹zole fetal asit olgular›n›n gebelik sürecinde nadiren spon-tan remisyona u¤rayabilece¤i bilinmeli, böyle bir olgunun saptan-mas› durumunda ileri tetkik ve tedavinin yap›labilece¤i perinatolo-ji merkezlerine refere edilmesinin önemi unutulmamal›d›r. Anahtar sözcükler: ‹zole fetal asit, ultrasonografi.

Correspondence: fiad›man K›ykaç Alt›nbafl, MD. Etlik Zübeyde Han›m Kad›n Hastal›klar›E¤itim ve Araflt›rma Hastanesi, Kad›n Hastal›klar› ve Do¤um Klini¤i, Dikmen, Ankara.e-mail: [email protected]





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nal center. In her first ultrasonography, single 26-weekfetus with common ascites in fetal abdomen wasobserved (Fig. 1). No pathologic indication wasdetected in fetus during ultrasonography and no renalor developmental defect was found. In Doppler ultra-sonography examination (umbilical artery Doppler,mid-cerebral artery Doppler), no pathology was found.Parvovirus B19, cytomegalovirus, toxoplasmosis, her-pes simplex, rubella, hepatitis A, B, and C infectionindicators of the patient were found as negative. Allother blood values of the patient were evaluated as nor-mal except anemia (hemoglobin: 11 g/dL).Karyotyping was done by taking sample amniotic fluidand karyotyping of the patient was reported as normal.

The patient and her family were informed in detailabout pathologies which cannot be detected althoughexamination results were found normal. In the follow-ups, fetus had severe fetal abdominal ascites until 35weeks gestation and fetal ascites had spontaneousremission at 36 weeks gestation. Healthy 4,200 grammale baby was delivered vaginally at 39 weeks gesta-tion. Examination findings of the newborn were foundas normal.

DiscussionFetal ascites can be defined as finding free fluid in fetalperitoneal cavity in ultrasonographic examination.Hydrops fetalis is the advanced state of these cases andit is free fluid accumulation in more than one compart-ment together with generalized edema. Non-immunefetal hydrops incidence varies between 1/1500 and1/4000.[4] Developmental pathologies are observed inthe background in most of the cases. Ascite pathologyfound in the fetus is a case which always requiresadvanced examination. Genetic (chromosomal or syn-drome associated) reasons are reported in case series ina range between 11% and 20%.[5,6] However, it is notpossible to determine accurate prevalence as limitednumber of case series is reported.

In the case series of Schmider et al. including 26patients, ascites was reported as the only diagnosis in 1patient while other cases were associated with differentanomalies.[3] In the cases series of El Bishry including12 patients with isolated fetal ascites who had no addi-tional anomalies in antenatal follow-up where fetalascites moving to hydrops were excluded from the

Fig. 1. Free abdominal fluid within fetal abdomen.


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study, fetal loss rate was found as 16.6% and itoccurred during antenatal follow-up in 30% of sponta-neous remission patients and after delivery in 20% ofpatients.[2] Similar to this rate, Boutall et al. reportedfetal loss rate as 17%.[6] In this series, fetal ascitesunderwent resolution in 3 of 5 patients (60%) duringantenatal follow-up and resolution occurred at postna-tal 2nd month in 1 patient.[6]

When it is evaluated together with other anomalies,perinatal mortality rates were reported as 57% and72%.[5,6] Our case was referred to our clinic foradvanced examination and treatment at her 26 weeksgestation from an external center, and in her examina-tions no additional pathology explaining fetal abdomi-nal ascites etiology was detected. In the antenatal fol-low-up of the patient, it was observed that fetal ascitescontinued until 36 weeks gestation and delivery wasdone at 39 weeks gestation. In this case, detecting noadditional anomaly and finding karyotype analysisgood as well as advanced gestational week were inter-preted as elements defining good prognosis. Nose et al.reported elements determining prognosis in isolatedfetal ascites cases as gestational week during diagnosisand the level of fetal abdominal distention.[7] Detectingascites presence before 24 weeks gestation and also thepresence of hydrops fetalis are shown among the badprognostic factors.[5]

Although the presence of fetal ascites is not anabsolute indication for elective cesarean, delivery tim-ing and obstetric risk management should be consid-ered as patient-specific. If ascites continues, it will beappropriate to plan delivery management togetherwith fetal abdominal circumference measurement.Analyzing cases with fetal ascites for elements withinthe etiology is quite essential in terms of follow-up andmanagement of patient and the information to be givento family. Multiple anomaly presence, hydrops fetalis,infection and cardiac anomalies are among the badprognostic factors associated with fetal loss (100%,80%, 71%, 91%, respectively).[6] In cases with isolatedfetal ascites, taking maternal blood (Parvovirus B19,toxoplasmosis, rubella, cytomegalovirus, herpes sim-plex, varicella, hepatitis) in terms of blood type andinfection indicators should be planned as well as the

detailed anamnesis. Intestine pathologies and cysticfibrosis should be researched in all cases with fetalascites. Displaying fetal growth by serial ultrasono-graphic measurements, evaluating the course of fetalascites, fetal anemia and following up placental suffi-ciency are essential. Families should be informed aboutpossible chromosomal anomalies and fetal karyotyp-ing. Also, it should be remembered that metabolic dis-eases which are hard to detect during antenatal periodmay progress with fetal ascites.[2]

ConclusionIt should be known that isolated fetal ascites casesrarely may have spontaneous remission during preg-nancy. However, when such a case is met, it should beremembered that an additional pathology may accom-pany most probably, and such cases should be referredto perinatology centers where advanced examinationand treatment can be carried out.


References1. Hadlock FP, Deter RL, Garcia-Pratt J, Athey P, Carpenter

R, Hinkley CM, et al. Fetal ascites not associated with Rhincompatibility: recognition and management with sonogra-phy. AJR Am J Roentgenol 1980;134:1225-30.

2. El Bishry G. The outcome of isolated fetal ascites. Eur JObstet Gynecol Reprod Biol 2008;137:43-6.

3. Schmider A, Henrich W, Reles A, Kjos S, Dudenhausen JW.Etiology and prognosis of fetal ascites. Fetal Diag Ther2003;18:230-6.

4. Henrich, W, Heeger J, Schmider A, Dudenhausen J.W.Complete spontaneous resolution of severe nonimmunolog-ical hydrops fetalis with unknown etiology in the secondtrimester – a case report. J Perinat Med 2005;30:522-7.

5. Favre R, Dreux S, Dommergues M, Dumez Y, Luton D,Qury JF, et al. Nonimmune fetal ascites: a series of 79 cases.Am J Obstet Gynecol 2004;190:407-12.

6. Boutall A, Urban MF, Stewart C. Diagnosis, etiology, andoutcome of fetal ascites in a South African hospital. Int JGynecol Obstet 2011;115:148-52.

7. Nose S, Usui N, Soh H, Kamiyama M, Tani G, KanagawaT, et al. The prognostic factors and the outcome of primaryisolated fetal ascites. Pediatr Surg Int 2011;27:799-804.

Interhemispheric arachnoid cyst associated withmeningomyelocele: a case report

Resul Ar›soy, Emre Erdo¤du, Oya Demirci, Oya Pekin, P›nar Kumru, Semih Tu¤rul

Department of Perinatology, Zeynep Kamil Maternity and Children Training and Research Hospital, Istanbul, Turkey

Introduction

Arachnoid cysts are cystic cavities filled with a fluid likecerebrospinal fluid and including collagen and cellwithin arachnoid membrane, and they comprise 1% ofintracranial lesions. Arachnoid cysts may exist in anypart of central nervous system including spinal canal.They are usually located on supratentorial and mid-line.[1,2] They rarely associated with other anomalies.

In this report, we discussed the diagnosis and man-agement of arachnoid cyst case associated withmeningomyelocele that we prenatally diagnosed.

Case ReportFetal biometric measurements of twenty-six years old,gravida 0, parity 0 patient without follow-up werefound consistent with 24 weeks, having normal amniot-ic fluid, placenta posterior located and with normalappearance in the routine fetal ultrasonographic exam-ination performed on 24 weeks gestation. In the crani-um examination, 21x21 mm hypoechoic cystic masswith normal margins is located at axial section, inter-hemispheric and even subthalamic level during the cra-nium examination (Fig. 1). No blood flow was observedin cystic mass during Doppler ultrasonographic exami-

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Abstract

Objective: To present a prenatally diagnosed case of interhemi-spheric arachnoid cyst associated with lumbosacral meningomye-locele and discussion of management for this case.

Case: A 26-year-old gravida 1, para 0 patient was referred to ourunit at 24 weeks gestation. A detailed ultrasound scan revealed a21x21 mm interhemispheric arachnoid cyst and lumbosacralmeningomyelocele. After counseling, termination of pregnancywas offered and accepted. The diagnosis was confirmed by post-mortem examination.

Conclusion: The presence of other anomalies should be investi-gated for the management of arachnoid cyst.

Key words: Interhemispheric arachnoid cyst, meningomyelocele,management.

Meningomiyeloselin efllik etti¤i interhemisferik araknoid kist: Olgu sunumu Amaç: Prenatal tan› alm›fl meningomiyeloselin efllik etti¤i interhe-misferik araknoid kist olgusunun sunulmas› ve yönetiminin tart›-fl›lmas› amaçlanm›flt›r.

Olgu: Yirmi alt› yafl›nda gravida 1, parite 0 olan gebenin 24. gebe-lik haftas›nda yap›lan detayl› ultrason muayenesinde 21x21 mmboyutlar›nda interhemisferik araknoid kist ve lumbosakral menin-gomiyelosel tespit edilmifltir. Aileye fetus hakk›nda dan›flmanl›kverildikten sonra gebeli¤in sonland›r›lmas› önerilmifl ve aile kabuletmifltir. Postmortem incelemede bulgular teyit edilmifltir.

Sonuç: Araknoid kist olgular›n›n yönetimi için di¤er anomalilerinvarl›¤› araflt›r›lmal›d›r.

Anahtar sözcükler: ‹nterhemisferik araknoid kist, meningomiye-losel, yönetim.

Correspondence: Resul Ar›soy, MD. Acibadem Cad. No:177 Zafer Apt. Daire: 12, Istanbul, Turkey.e-mail: [email protected]






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nation. Posterior lateral ventricle was measured as 8.7mm, cerebellum as 24 mm and cistern magna as 2 mm.Also, cavum septum pellucidum was observed but nocorpus callosum was seen positionally. In the columnavertebralis examination, 43x31 mm meningomyelocelewas found in lumbosacral area (Fig. 2).

No additional anomaly was found in other systemexaminations of fetus. Anomalies were confirmed byfetal MRI (Fig. 3) and corpus callosum agenesia wasruled out. The family was informed about fetus andtermination of pregnancy after karyotype analysis wasoffered to the family as an option. The result of kary-otype analysis was 46 XY and in the pathological exam-ination of fetus, 25x25 mm cystic mass and 50 mmlumbosacral meningomyelocele were found on supra-tentorial region in middle interhemispheric area. It wasreported that hyperplastic arachnoid cells wereobserved in the microscopic analysis of the cyst andantenatal diagnosis was confirmed.

DiscussionArachnoid cysts comprise 1% of intracranial lesions.They appear as congenital (primary) or associated withbleeding, trauma and infection (secondary). Congenitalones appear between 6 and 8 weeks gestation duringhemispheric folding and arachnoid membrane separa-tion. More than 50% of arachnoid cysts are located

middle fossa in supratentorial region. Other intenselocalizations are major fissures (silvian, rolandic andinterhemispheric), surfaces of cerebral hemispheres,sella turcica region and anterior fossa.[1-4]

In our case, interhemispeheric located arachnoidcyst at 24 weeks gestation was presented. Most of thearachnoid cyst cases were diagnosed at the end of sec-ond trimester.[5] The earliest diagnosis of arachnoidcyst was reported by Bretelle et al. at 13 weeks gesta-tion by transvaginal ultrasonography.[1]

The differential diagnosis should be done for arach-noid cyst by porencephalic cyst which may be inintracranial hypoechoic lesion appearance, glioependi-mal cyst, choroid plexus cyst, vein of Galen aneurysm,schizencephaly, cystic neoplasm and intracranial hem-orrhage.[6] Arachnoid cysts are seen as hypoechoic cys-tic mass which has regular margins in ultrasonographyand no blood flow in Doppler examination.[6,7] MRI canbe beneficial for both differential diagnosis and scan-ning accompanying anomalies.[8] Arachnoid cyst is usu-ally isolated and seems to be associated with ventricu-lomegaly and corpus callosum agenesis.[5,6,8]

In our case, arachnoid cyst seems associated withmeningomyelocele but association was not found inthe literature. Akdemir et al.[9] and Gedikbafl› et al.[10]

reported that arachnoid cyst grows as gestational weekincreases and they may cause ventriculomegaly. Pilu et

Fig. 1. The appearance of interhemispheric arachnoid cyst on axial plane.

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al. reported associated corpus callosum agenesis in twoof seven arachnoid cyst cases (great arachnoid cyst caseon midline located on anterior fossa and two arachnoidcyst cases which are 5 mm and 6 mm in ambient cis-

tern).[6] In the case presented by Elbers and Furness,they diagnosed arachnoid cyst at 18.5 weeks gestation,and they reported that cyst regressed at 32 weeks ges-tation and then disappeared.[11]

Karyotype is normal in most of the arachnoid cystcases, but karyotyping analysis is recommended in iso-lated cases. Pilu et al. found trisomy 18 in karyotypeanalysis of an arachnoid cyst case located in ambientcistern associated with right ventricle with double out-let and nodular hand diagnoses.[6] Hoge et al. reportedthe association of infratentorial arachnoid cyst casewith partial trisomy 9q (9q22_qter) and partial mono-somy Xq (Xq22_qter) (12). Souter et al. found mono-somy 14q (14q32.3_qter) in midline intracranial arach-noid cyst case accompanied with fallot's tetralogy andintrauterine growth.[13]

ConclusionFor the management of arachnoid cyst cases, presenceof all other anomalies that may accompany should beresearched. Karyotype analysis and termination ofpregnancy may be recommended in the presence ofmultiple anomalies. Prognosis is good in isolated cases,but they should be followed up in terms of cyst size andobstructive ventriculomegaly.


Fig. 2. The appearance of meningomyelocele on axial plane.

Fig. 3. The appearance of interhemispheric arachnoid cyst on axialplane by MRI.


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References1. Bretelle F, Senat MV, Bernard JP, Hillion Y, Ville Y. First-

trimester diagnosis of fetal arachnoid cyst: prenatal implica-tion. Ultrasound Obstet Gynecol 2002;20:400-2.

2. Chen CP. Prenatal diagnosis of arachnoid cysts. Taiwan JObstet Gynecol 2007;46:187-98.

3. Choi JU, Kim DS. Pathogenesis of arachnoid cyst: congeni-tal or traumatic? Pediatr Neurosurg 1998;29:260-6.

4. Wester K. Peculiarities of intracranial arachnoid cysts: loca-tion, sidedness, and sex distribution in 126 consecutivepatients. Neurosurgery 1999;45:775-9.

5. Langer B, Haddad J, Favre R, Frigue V, Schlaeder G. Fetalarachnoid cyst: report of two cases. Ultrasound ObstetGynecol 1994;4:68-72.

6. Pilu G, Falco P, Perolo A, Sandri F, Cocchi G, Ancora G, etal. Differential diagnosis and outcome of fetal intracranialhypoechoic lesions: report of 21 cases. Ultrasound ObstetGynecol 1997;9:229-36.

7. Barjot P, von Theobald P, Refanhi N, Delautre V,Herlicoviez M. Diagnosis of arachnoid cysts on prenatalultrasound. Fetal Diagn Ther 1999;14:306-9.

8. Blaicher W, Prayer D, Kuhle S, Deutinger J, Bernaschek G.Combined prenatal ultrasound and magnetic resonanceimaging in two fetuses with suspected arachnoid cysts.Ultrasound Obstet Gynecol 2001;18:166-8.

9. Akdemir N, Altunyurt S, Uysal D, Yüceer N. Fetalintrakraniyal kistik görünümlü kitle saptanan iki olgu: tan›,takip ve prognoz. Turkiye Klinikleri Journal of Gynecologyand Obstetrics 2009;19:231-5.

10. Gedikbasi A, Palabiyik F, Oztarhan A, Yildirim G, Eren C,Ozyurt SS, et al. Prenatal diagnosis of a suprasellar arach-noid cyst with 2- and 3-dimensional sonography and fetalmagnetic resonance imaging: difficulties in management andreview of the literature. J Ultrasound Med 2010;29:1487-93.

11. Elbers SE, Furness ME. Resolution of presumed arachnoidcyst in utero. Ultrasound Obstet Gynecol 1999;14:353–5.

12. Hogge WA, Schnatterly P, Ferguson JE 2nd. Early prenataldiagnosis of an infratentorial arachnoid cyst: association withan unbalanced translocation. Prenat Diagn 1995;15:186-8.

13. Souter VL, Glass IA, Chapman DB, Raff ML, Parisi MA,Opheim KE, et al. Multiple fetal anomalies associated withsubtle subtelomeric chromosomal rearrangements.Ultrasound Obstet Gynecol 2003;21:609-15.

Bilateral type 1 congenital cystic adenomatoid malformation: a case report

Resul Ar›soy, Emre Erdo¤du, Oya Pekin, Oya Demirci, P›nar Kumru, Semih Tu¤rul

Department of Perinatology, Ministry of Health Zeynep Kamil Maternity and Child Training and Research Hospital, Istanbul, Turkey

IntroductionCongenital cystic adenomatoid malformation (CCAM)is a hamartomatous lung lesion characterized by theproliferation of terminal bronchioles and abnormalalveolar development.[1,2] Its etiology has not been

revealed yet, and it has been found out that it has a rolein the pathology of increased apoptosis and that it isassociated with HOXB5, FGF7, and PDGFB genes.[3,4]

The malformation was first grouped in three typesaccording to the sizes of cysts by Stocker in 1977.[5]

Case Report��

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Bilateral Tip 1 konjenital kistik adenomatoid malformasyon: Olgu sunumuAmaç: Prenatal tan› alm›fl bilateral Tip 1 konjenital kistik adeno-matoid malformasyon olgusunun sunulmas› ve yönetiminin tart›-fl›lmas› amaçlanm›flt›r.

Olgu: Yirmi yedi yafl›nda gravida 4, parite 2, abort 1 olan gebe25+5 gebelik haftas›nda hidrops fetalis ön tan›s› nedeniyle klini¤i-mize refere edilmifltir. Fetüsün de¤erlendirilmesinde bilateral ak-ci¤erlerde en büyü¤ü 26x24 mm boyutlar›nda multiloküler aneko-ik kistik yap›lar, kalp aks›n›n sola kayd›¤› ve yo¤un assit saptand›.Di¤er sistemlerin muayenesinde ek anomali saptanmad›. Tip 1konjenital kistik adenomatoid malformasyon ön tan›s› konularak;aile fetüsün prognozu aç›s›ndan bilgilendirildi ve gebeli¤in termi-nasyonu bir seçenek olarak sunuldu. Postmortem patoloji incele-mesinde de tan› do¤ruland›.

Sonuç: Tip 1 konjenital kistik adenomatoid malformasyon olgula-r›n›n ay›r›c› tan›s› ve efllik eden di¤er anomalilerin varl›¤› yönetimaç›s›ndan önemlidir. Erken fetal hidropsun efllik etti¤i bilateralTip 1 konjenital kistik adenomatoid malformasyon olgular›ndaprognoz kötü olup; gebeli¤in tahliyesi önerilebilir.

Anahtar sözcükler: Bilateral konjenital kistik adenomatoid mal-formasyon, prenatal tan›, yönetim.

Abstract

Objective: It is aimed to present a case of bilateral type 1 congen-ital cystic adenomatoid malformation which is prenatally diag-nosed, and to discuss the management in these cases.

Case: A 27-year-old, gravida 4, parity 2, abort 1 patient wasreferred to our clinic with an initial diagnosis of hydrops fetalis at25+5 weeks gestation of pregnancy. In the evaluation of fetus, itwas detected by ultrasonography that bilateral pulmonary multi-locular anechoic cystic lesions which were measured as maximum24x26 mm were present, cardiac axis shifted to left, and commonascites were present. No additional anomaly was detected duringthe examinations of other systems. After the diagnosis of type 1congenital cystic adenomatoid malformation, parents wereinformed about the fetal prognosis and termination of pregnancywas put forward as an option. Diagnosis was confirmed by thepostmortem pathological examination.

Conclusion: The differential diagnosis of type 1 congenital cysticadenomatoid malformation and the presence of concomitantanomalies are important for the management of these cases. Theprognosis is poor in cases with bilateral type 1 congenital cysticadenomatoid malformation accompanied by early hydrops fetalis,and the termination of pregnancy can be offered.

Key words: Bilateral congenital cystic adenomatoid malforma-tion, prenatal diagnosis, management.

Correspondence: Resul Ar›soy, MD. Ac›badem Cad. No: 177 Zafer Apt. Daire: 12, Istanbul, Turkey.e-mail: [email protected]

Received: October 18, 2012; Accepted: December 21, 2012





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In 2002, Stocker updated CCAM classification asfive types by adding Type 0 and Type 4. Type 0 issmall cystic lethal lesions arising from trachea andbronchus, and it is quite rare. Type 1 consists of 50-70% of CCAM cases and it includes cystic lesionswhich are 3-10 cm in size arising from distal bronchusand proximal bronchioles. Type 2 is the group having0.5-2 cm lesions arising from terminal bronchiolesand/or accompanied by solid lesions. Type 2 is 15-30%of CCAM cases and it is the group which is the mostassociated one (60%) with other system anomalies.Type 3 is caused by acinar tissue and includes micro-cystic solid hyperechogenic lesions; it constitutes 5-10% of CCAM cases. Type 4 is caused by alveolar tis-sue and it includes ≥10 cm cystic lesions; it is 5-15% ofCCAM cases and it is particularly associated with pleu-ropulmonary blastoma.[6]

Adzick et al. categorized CCAM into two groupsaccording to their ultrasonographic views, which aremicrocystic (<5 mm cystic or solid lesions) and macro-cystic (>5 mm cystic lesions) types.[7] Most of theCCAM cases are unilateral, and they are lesions limit-ed with single lobe of lungs.

By this report, we aimed to discuss the diagnosisand management of the case of bilateral type 1 congen-ital cystic adenomatoid malformation accompanied byhydrops fetalis diagnosed at second trimester.

Case ReportA 27-year-old, gravida 4, parity 2, abort 1 patient wasreferred to our clinic with an initial diagnosis of

hydrops fetalis at 25+5 weeks gestation no medical andobstetric problem was found in her history. Thebiparietal diameter of the fetus was measured 65 mm,head circumference 254 mm, femur length 46 mm,abdominal circumference 342 mm (>97 percentile) andamniotic fluid index 200 mm during ultrasonographicexamination. It was detected during fetus examinationthat there were multilocular anechoic cystic lesions(Figs. 1-3) which were maximum 26x24 mm, that car-diac axis shifted to left (85 degrees), and commonascites (Fig. 4) as well as skin edema and hydrocelewere present. No additional anomaly was found duringthe examination of other systems. The pre-diagnosis ofbilateral type 1 congenital cystic adenomatoid malfor-mation accompanied by hydrops fetalis was estab-lished. The family was informed in terms of examina-tion findings of fetus and the prognosis and it wasoffered to terminate the pregnancy. The consent of thepatient was taken. Intracardiac potassium was appliedto fetus. By inducting 400 μg intravaginal misoprostolapplication, 1650 gram male fetus in hydropic view wasdelivered with negative heartbeat. Hydrops fetalis andCCAM diagnoses were confirmed in postmortempathology examination. No additional histopathologi-cal diagnosis was detected.

DiscussionThe frequency of congenital cystic adenoid malforma-tion is 1/11.000 – 35.000, and 80-95% of cases are uni-lateral and associated with single lobe of lungs.[8,9]

CCAM is diagnosed as echogenic lesions in lungs which

Fig. 1. Bilateral type 1 CCAM view on transverse section. Fig. 2. Type 1 CCAM view in right lung on sagittal section.

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are solid, cystic or including both forms during ultra-sonographic examination at second trimester.[8-11]

Gornall et al. reported that the accuracy of ultrasonog-raphy for CCAM at prenatal period is 81% and the pos-itive predictive value is 57%.[9] In order to decrease theerror rate in prenatal diagnosis of CCAM, differentialdiagnosis for diaphragmatic hernia, extralobar andintralobar bronchopulmonary sequestration, lobaremphysema, bronchogenic cyst, and mediastinal lesionssuch as cystic teratoma or neurenteric cyst.[8-12] In differ-ential diagnosis, Doppler ultrasonography and especial-ly fetal MRI during advanced gestational weeks arehelpful. The association of CCAM with bronchopul-monary sequestration, tracheal obstruction, bronchialatresia and lobar emphysema is not rare.[10]

Illanes et al. conducted a study including 43 CCAMcases and found out that 56% of cases had macrocysticlesions (>5 mm), 67% of them had mediastinal shift,and 19% of them had hydrops fetalis. Also, mortalityrate of cases developing hydrops was reported as75%.[10] Ierullo et al. examined 34 CCAM cases and theyreported that 20.6% of the cases were macrocystic andall of them were unilateral, 79.4% of them had medi-astinal shift and hydrops developed in 17.6% of them.[11]

In our case, we detected that there were macrocysticmultiocular lesions in bilateral lungs, cardiac axis shift-ed to left and there was hydrops.

Calvert et al. also found out that their all CCAMcases were unilateral and hydrops developed in 8.7% ofthem. In 48% of CCAM cases had regression duringantenatal period and also 8.7% of the cases had com-plete regression.[13] CCAM is isolated and it rarely asso-

ciates with other structural anomalies. However, theassociation of type 2 CCAM cases with cardiac (truncusarteriosus and Fallot's tetralogy) or renal anomalies, gas-trointestinal system atresias and skeletal dysplasias.[8-14]

The relationship of CCAM cases with chromosomalanomalies is not known. Follow-up and management ofCCAM cases should be planned according to gestation-al week, CCAM volume (calculated by the formula ofheight x length x width x 0.52 for lesion after ultrasono-graphic image of CCAM is obtained) or CVR rate(CCAM volume/head circumference). If CVR is higherthan 1.6, then fetal hydrops risk is high and it is recom-mended to carry out fetal evaluation three times a week;if it is lower than 1.2, then it is recommended to carryout fetal evaluation once a week.[16-18] It was reportedthat CRV displayed a rapid increase between 20 and 25weeks gestation and decrease after 25 weeks gestation,and it was highlighted that follow-ups during theseweeks are significant.[16]

The presence of mediastinal shift, amniotic fluidindex, umbilical artery Doppler flow pattern, ductusvenosus Doppler flow pattern and placental thicknessare used as the other significant parameters in fetal fol-low-up. Prognosis is generally better in type 1 CCAMcases, but the prognosis is poor in the presence ofhydrops fetalis, ascites, polyhydramniosis, bilateral lunginvolvement and mediastinal shift.[8-13,15] Isolated casesnot accompanied by hydrops should be evaluated byfollow-up parameters once every three weeks.[8] In caseswith CCAM including single or multiple major cysticlesions and accompanied by hydrops cases, it was shownthat thoracoamniotic shunt is useful if gestational week

Fig. 3. Type 1 CCAM view in left lung on sagittal section. Fig. 4. The view of ascites on transverse section.


Bilateral type 1 congenital cystic adenomatoid malformation

163

is lower than 32 after the presence of other structuraland chromosomal anomalies is excluded. However, itwas reported that thoracocentesis is not effective andcystic substance accumulated again in a short time.Thoracoamniotic shunt is not recommended in thepresence of multicystic or semisolid or weighted solidlesions. It is suggested to plan delivery after 32 weeksgestation.[17,18]

In our case, thoracoamniotic shunt was not consid-ered due to the presence of multiple cystic lesions inbilateral lungs and family discord. Upon the request offamily, pregnancy was terminated with the diagnoses ofbilateral type 1 CCAM and hydrops fetalis.

ConclusionThe differential diagnosis of type 1 congenital cysticadenomatoid malformation cases and presence of otheraccompanying anomalies are significant in terms ofmanagement. Prognosis is better in isolated type 1congenital cystic adenomatioid malformation cases,and they can be followed up conservatively. In cases ofmulticystic bilateral type 1 congenital cystic adenoma-toid malformation, prognosis is poor in the presence ofhydrops fetalis, ascites, polyhydramniosis and medi-astinal shift, and termination of pregnancy can be rec-ommended.


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Papakonstantinou K, Kondi-Pafiti A. Congenital cystic ade-nomatoid lung malformation: report of two cases and litera-ture review. Clin Exp Obstet Gynecol 2008;35:76-80.

2. Schott S, Mackensen-Haen S, Wallwiener M, Meyberg-Solomayer G, Kagan KO. Cystic adenomatoid malformationof the lung causing hydrops fetalis: case report and review ofthe literature. Arch Gynecol Obstet 2009;280:293-6.

3. Volpe MV, Pham L, Lessin M, Ralston SJ, Bhan I, Cutz E,

et al. Expression of Hoxb-5 during human lung developmentand in congenital lung malformations. Birth Defects Res AClin Mol Teratol 2003;67:550-6.

4. Jancelewicz T, Nobuhara K, Hawgood S. Laser microdissec-tion allows detection of abnormal gene expression in cysticadenomatoid malformation of the lung. J Pediatr Surg2008;43:1044-51.

5. Stocker JT, Madewell JE, Drake RM. Congenital cystic ade-nomatoid malformation of the lung. Classification and mor-phologic spectrum. Hum Pathol 1977;8:155-71.

6. Stocker JT. Congenital pulmonary airway malformation – anew name for and an expanded classification of congenitalcystic adenomatoid malformation of the lung.Histopathology 2002;41424-31.

7. Adzick NS, Harrison MR, Glick PL, Globus MS, AndersonRL, Mahony BS, et al. Fetal cystic adenomatoid malforma-tion: prenatal diagnosis and natural history. J Pediatr Surg1985;20:483-8.

8. Sfakianaki AK, Copel JA. Congenital cystic lesions of thelung: congenital cystic adenomatoid malformation and bron-chopulmonary sequestration. Rev Obstet Gynecol 2012;5:85-93.

9. Gornall AS, Budd JL, Draper ES, Konje JC, Kurinczuk JJ.Congenital cystic adenomatoid malformation: accuracy ofprenatal diagnosis, prevalence and outcome in a general pop-ulation. Prenat Diagn 2003;23:997-1002.

10. Illanes S, Hunter A, Evans M, Cusick E, Soothill P. Prenataldiagnosis of echogenic lung: evolution and outcome.Ultrasound Obstet Gynecol 2005;26:145-9.

11. Ierullo AM, Ganapathy R, Crowley S, Craxford L, Bhide A,Thilaganathan B. Neonatal outcome of antenatally diag-nosed congenital cystic adenomatoid malformations.Ultrasound Obstet Gynecol 2005;26:150-3.

12. Lecomte B, Hadden H, Coste K, Gallot D, Laurichesse H,Lemery D, et al. Hyperechoic congenital lung lesions in anon-selected population: from prenatal detection till perina-tal management. Prenat Diagn 2009;29:1222-30.

13. Calvert JK, Boyd PA, Chamberlain PC, Syed S, Lakhoo K.Outcome of antenatally suspected congenital cystic adeno-matoid malformation of the lung: 10 years' experience 1991-2001. Arch Dis Child Fetal Neonatal Ed 2006;91:26-8.

14. Orpen N, Goodman R, Bowker C, Lakhoo K. Intralobarpulmonary sequestration with congenital cystic adematousmalformation and rhabdomyomatous dysplasia. Pediatr SurgInt 2003;19:610-1.

Perinatal Journal164

A case of heterotopic pregnancy in a spontaneous cycle. Cihan-gir Mutlu Ercan, Mehmet Sak›nc›, U¤ur Keskin, Hakan Çoksüer,Ercan Bal›kç›, Ali Ergün. 20(2):63-67 [Case Report]

Agenesis of ductus venosus: a case report. Talat Umut Kutlu Di-lek, Burcu Dilek. 20(3):150-152 [Case Report]

Analysis of the relationship between maternal second trimesterAFP, HCG, estriol levels and uterine artery Doppler findings inthe prediction of pregnancy complications. Banu Dane, GoncaBatmaz, Kamuran K›lavuz, Yaprak Rüstemo¤lu, Hande Güler, CemDane. 20(1):24-29 [Research Article]

Apert syndrome: a case report. ‹brahim Alanbay, Hakan Çoksüer,Emre Karaflahin, Mutlu Ercan, U¤ur Keskin, Seyit Temel Ceyhan,‹skender Bafler. 20(1):30-34 [Case Report]

Bilateral type 1 congenital cystic adenomatoid malformation: acase report. Resul Ar›soy, Emre Erdo¤du, Oya Pekin, Oya Demir-ci, P›nar Kumru, Semih Tu¤rul. 20(3):160-163 [Case Report]

Can a temporary isolated fetal megacystis during first trimesterresult in unexplained intrauterine fetal death at third trimester?A case report and review of the literature. Servet Hac›velio¤lu,Ayflenur Çak›r Güngör, Meryem Gencer, Emine Coflar. 20(2):68-71[Case Report]

Determination of the median levels of first trimester screeningtest parameters in our region. Dilek Beker fianl›, Kaz›m Kartkaya.20(1):6-11 [Research Article]

Evaluation of platelet count and platelet function in intrahepat-ic cholestasis of pregnancy. Mehmet S›dd›k Evsen, Hatice EnderSoydinç, Ali Özler, Serdar Baflarano¤lu, Talip Karaçor, Ahmet Ya-l›nkaya, Derya Uçmak, Muhsin Kaya. 20(2):45-48 [ResearchArticle]

Evaluation of prenatal care in Istanbul: a population basedstudy. Binali Çatak, Hatice ‹ki›fl›k, Savafl Baflar Kartal, Can Öner,Handan Hazal Uluç, Özgür Se¤men. 20(3):126-134 [Case Report]

Evaluation of the perinatal results of pregnant with pretermpremature rupture of membrane. Orkun Çetin, ‹pek Dokurel Çe-tin, Cihat fien, Seyfettin Uluda¤, Begüm Aydo¤an, Abdullah Tüten.20(2):49-54 [Research Article]

Importance of perinatal vitamin D prophylaxis for mother andthe newborn. Ali Kaya, Ahmet Sami Güven, As›m Gültekin, FüsunDilara ‹ça¤as›o¤lu, Ömer Cevit. 20(1):18-23 [Research Article]

Interhemispheric arachnoid cyst associated with meningomye-locele: a case report. Resul Ar›soy, Emre Erdo¤du, Oya Demirci,Oya Pekin, P›nar Kumru, Semih Tu¤rul. 20(3):156-159 [CaseReport]

Investigation of the relationship between levels of oxidativestress markers in the second trimester amniotic fluid with

preeclampsia and preterm delivery. Ebru Çelik, Abdullah Karaer,Ercan Y›lmaz, Ilg›n Türkçüo¤lu, Önder Çelik, Yavuz fiimflek, P›narK›r›c›, Elif Özerol, Kevser Tanbek. 20(3):140-145 [Case Report]

Ovarian cyst rupture during real-time transvaginal Dopplerultrasonography. Mekin Sezik. 20(3):146-149 [Case Report]

Patient profile and treatment outcomes of (near-miss) obstetricpatients and evaluation of maternal mortality: a tertiary centerexperience. Ömer Yavuz fiimflek, Ercan Y›lmaz, Ebru Çelik, Abdul-lah Karaer, Ilg›n Türkçüo¤lu, Önder Çelik, Türkan To¤al. 20(1):1-5 [Research Article]

Recurrent lethal multiple pterygium syndrome: prenatal ultra-sonographic and postmortem findings. Cihangir Mutlu Ercan,Sertaç Esin, Hakan Çoksüer, Özcan Özkan, ‹brahim Alanbay, ‹sken-der Bafler. 20(1):35-39 [Case Report]

Retrospective analysis of maternal and fetal outcomes in preg-nant women with chronic immune thrombocytopenic purpura.Hatice Ender Soydinç, Muhammet Erdal Sak, Mehmet S›dd›k Evsen,Ali Özler, Abdülkadir Turgut, Serdar Baflarano¤lu, Talip Gül.20(1):12-17 [Case Report]

Retrospective analysis of stillbirth cases in a regional hospital.Muhammet Erdal Sak, Mehmet S›dd›k Evsen, Hatice Ender Soy-dinç, Sibel Sak, Serdar Baflarano¤lu, Ahmet Yal›nkaya. 20(3):135-139 [Research Article]

Sequential therapy failure in a naturally concieved twin preg-nancy complicated by reversed arterial perfusion. Ömer Yavuzfiimflek, Önder Çelik, Ercan Y›lmaz, Ebru Çelik, Senem Arda Düz,Serdar Ceylaner, fievki Çelen, Nuri Dan›flman. 20(1):40-44 [CaseReport]

Sirenomelia: a case report. Bülent Demir, Ali ‹rfan Güzel, Sürey-ya Demir, Nihal K›l›nç. 20(2):59-62 [Case Report]

Sonographically documented spontaneous resolution of isolat-ed fetal ascites. fiad›man K›ykaç Alt›nbafl, Ömer Kandemir, SerdarYalvaç, Ümit Göktolga. 20(3):153-155 [Case Report]

The giant fetal axillary lymphangioma showing good prognosis.Hatice Ender Soydinç, Neval Yaman Görük, Abdulkadir Turgut,Ça¤lar Altundal, Serdar Baflarano¤lu, Ahmet Yal›nkaya. 20(2):72-75[Case Report]

The impact of fetal inflammatory response syndrome on peri-natal outcomes in cases of preterm premature rupture of mem-branes. Orkun Çetin, ‹pek Dokurel Çetin, Onur Güralp, Cihat fien,Seyfettin Uluda¤, Ali Galip Zebitay. 20(3):121-125 [ResearchArticle]

The operative vaginal delivery: experience of five years. OrkunÇetin, ‹pek Dokurel Çetin, Cihat fien, Seyfettin Uluda¤, Ali GalipZebitay, O¤uz Yücel. 20(2):55-58 [Research Article]

Subject Index(Volume 20, 2012)

Subject Index��

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Volume 20 | Issue 3 | December 2012 165

Author Index(Volume 20, 2012)

(The bold typed references are the ones in which the person is the first author.)

Author Index��

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AAlanbay ‹. 30, 35Altundal Ç. 72Arda Düz S. 40Ar›soy R. 156, 160Aydo¤an B. 49

BBal›kç› E. 63 Baflarano¤lu S. 12, 45, 72, 135 Bafler ‹. 30, 35Batmaz G. 24Beker fianl› D. 6

CCevit Ö. 18Ceyhan S.T. 30 Ceylaner S. 40Coflar E. 68

ÇÇak›r Güngör A. 68Çatak B. 126 Çelen fi. 40Çelik E. 1, 40, 140Çelik Ö. 1, 40, 140, Çetin O. 45, 49, 121Çoksüer H. 30, 35, 63

DDane B. 24Dane C. 24 Dan›flman N. 40Demir B. 59Demir S. 59Demirci O. 156, 160 Dilek B. 150 Dilek T.U.K 150Dokurel Çetin ‹. 45, 49, 121

EEnder Soydinç H. 12, 45, 72, 135Ercan C.M. 35, 63Ercan M. 30Erdo¤du E. 156, 160

Ergün A. 63 Esin S. 35 Evsen M.S. 12, 45, 135,

GGencer M. 68Göktolga Ü. 153 Gül T. 12Güler H. 24 Gültekin A. 18Güralp O. 121Güven A.S. 18Güzel A.‹. 59

HHac›velio¤lu S. 68

IIlg›n Türkçüo¤lu I. 1

‹‹ça¤as›o¤lu F.D. 18‹ki›fl›k H. 126

KKandemir Ö. 153Karaçor T. 45Karaer A. 1, 140 Karaflahin E. 30Kartal S.B. 126Kartkaya K. 6Kaya M. 45Keskin U. 30, 63 K›lavuz K. 24 K›l›nç N. 59K›r›c› P. 140 Kaya A. 18K›ykaç Alt›nbafl fi. 153 Kumru P. 156, 160

ÖÖner C.126Özerol E. 140 Özkan Ö. 35Özler A. 12, 45

PPekin O. 156, 160

RRüstemo¤lu Y. 24

SSak M.E. 12, 135Sak S. 135Sak›nc› M. 63 Se¤men Ö. 126Sezik M. 146

fifien C. 45, 49, 121fiimflek Ö.Y. 1, 40, 140

TTanbek K. 140 To¤al T. 1 Tu¤rul S. 156, 160 Turgut A. 12, 72Türkçüo¤lu I. 140 Tüten A. 49

UUçmak D. 45 Uluç H.H. 126Uluda¤ S. 45, 49, 121

YYal›nkaya A. 4, 72, 135 Yalvaç S. 153Yaman Görük N. 72Y›lmaz E. 1, 40, 140 Yücel O. 45

ZZebitay A.G. 45, 121

Perinatal Journal166

Olufl Api

‹nan ‹lker Ar›kan

Yeflim Baytur

Ebru Çelik

Rahime Nida Ergin

Ali Ergün

Ayse Kafkasl›

N. Ömer Kandemir

Mertihan Kurdo¤lu

Nilgün Kültürsay

Murat Muhcu

Ercüment Müngen

Soner Recai Öner

Lütfü Öndero¤lu

Mehmet Özeren

Mehmet Okan Özkaya

Özlem Pata

Turgay fiener

H. Alper Tanr›verdi

Ahmet Yal›nkaya

Murat Yayla

Reviewer Index(Volume 20, 2012)

The Editorial Staff of the Perinatal Journal expresses their appreciation to the follouing colleagues who have reviewed manuscripts for Volume 20, 2012.*

Reviewer Index��

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*Names are in alphabetical order.

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